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26 Fluid, Electrolyte, and Acid-Base Balance
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Infants: 73% or more water (low body fat, low bone mass)
Body Water Content Infants: 73% or more water (low body fat, low bone mass) Adult males: ~60% water Adult females: ~50% water (higher fat content, less skeletal muscle mass) Adipose tissue least hydrated of all Water content declines to ~45% in old age © 2013 Pearson Education, Inc.
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Two main fluid compartments
Total body water = 40 L Two main fluid compartments Intracellular fluid (ICF) compartment: 2/3 in cells Extracellular fluid (ECF) compartment: 1/3 outside cells Plasma: 3 L Interstitial fluid (IF): 12 L in spaces between cells Usually considered part of IF: lymph, CSF, humors of the eye, synovial fluid, serous fluid, and gastrointestinal secretions © 2013 Pearson Education, Inc.
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Intracellular fluid (ICF) Volume = 25 L 40% of body weight Plasma
Figure The major fluid compartments of the body. Total body water Volume = 40 L 60% of body weight Interstitial fluid (IF) Volume = 12 L 80% of ECF Intracellular fluid (ICF) Volume = 25 L 40% of body weight Plasma Volume = 3 L, 20% of ECF Extracellular fluid (ECF) Volume = 15 L 20% of body weight © 2013 Pearson Education, Inc.
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Composition of Body Fluids
Water: universal solvent Solutes: what is dissolved in water Classified as nonelectrolytes and electrolytes Nonelectrolytes: most organic Do not dissociate in water: e.g., glucose, lipids, creatinine, and urea No charged particles created © 2013 Pearson Education, Inc.
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Composition of Body Fluids
Electrolytes Dissociate into ions in water; e.g., inorganic salts, all acids and bases, some proteins Ions conduct electrical current Greater osmotic power than nonelectrolytes Greatest ability to cause fluid shifts © 2013 Pearson Education, Inc.
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Electrolyte Concentration
© 2013 Pearson Education, Inc.
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Electrolyte Concentration
For single charged ions (e.g. Na+), 1 mEq = 1 mOsm For bivalent ions (e.g. Ca2+), 1 mEq = 1/2 mOsm 1mEq of either provides same amount of charge © 2013 Pearson Education, Inc.
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Extracellular and Intracellular Fluids
Each fluid compartment has distinctive pattern of electrolytes ECF All similar Major cation: Na+ Major anion: Cl– Except: higher protein, lower Cl– content of plasma © 2013 Pearson Education, Inc.
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Extracellular and Intracellular Fluids
ICF: Low Na+ and Cl– Major cation: K+ Major anion HPO42– More soluble proteins than in plasma © 2013 Pearson Education, Inc.
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Extracellular and Intracellular Fluids
Electrolytes most abundant solutes in body fluids; determine most chemical and physical reactions Bulk of dissolved solutes are proteins, phospholipids, cholesterol, and triglycerides 90% in plasma 60% in IF 97% in ICF © 2013 Pearson Education, Inc.
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Total solute concentration (mEq/L)
Figure Electrolyte composition of blood plasma, interstitial fluid, and intracellular fluid. 160 140 120 Blood plasma Interstitial fluid Intracellular fluid 100 Na+ Sodium Total solute concentration (mEq/L) 80 K+ Potassium Ca2+ Calcium Mg2+ Magnesium 60 HCO3– Bicarbonate Cl– Chloride HPO42– Hydrogen phosphate 40 SO42– Sulfate 20 Na+ K+ Ca2+ Mg2+ HCO3– Cl– HPO42– SO42– Protein anions © 2013 Pearson Education, Inc.
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Fluid Movement Among Compartments
Osmotic and hydrostatic pressures regulate continuous exchange and mixing of fluids Water moves freely along osmotic gradients All body fluid osmolality almost always equal Change in solute concentration of any compartment leads to net water flow ECF osmolality water leaves cell ECF osmolality water enters cell © 2013 Pearson Education, Inc.
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Fluid Movement Among Compartments
Between plasma and IF across capillary walls Fluid leaks from arteriole end of capillary, reabsorbed at venule end; lymphatics pick up remaining and return to blood Between IF and ICF across cell membrane Two-way osmotic flow of water Ions move selectively; nutrients, wastes, gases unidirectional © 2013 Pearson Education, Inc.
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Lungs Gastrointestinal Kidneys tract Blood O2 CO2 Nutrients H2O, H2O,
Figure Exchange of gases, nutrients, water, and wastes between the three fluid compartments of the body. Lungs Gastrointestinal tract Kidneys Blood plasma O2 CO2 Nutrients H2O, Ions H2O, Ions Nitrogenous wastes O2 CO2 Nutrients H2O Ions Nitrogenous wastes Interstitial fluid Intracellular fluid in tissue cells © 2013 Pearson Education, Inc.
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Water Balance and ECF Osmolality
Water intake must = water output = ~ 2500 ml/day Water intake: beverages, food, and metabolic water Water output: urine (60%), insensible water loss (lost through skin and lungs), perspiration, and feces © 2013 Pearson Education, Inc.
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100 ml Feces 4% Metabolism 10% 250 ml Sweat 8% 200 ml Insensible loss
Figure Major sources of water intake and output. 100 ml Feces 4% Metabolism 10% 250 ml Sweat 8% 200 ml Insensible loss via skin and lungs 28% Foods 30% 750 ml 700 ml 2500 ml Urine 60% Beverages 60% 1500 ml 1500 ml Average intake per day Average output per day © 2013 Pearson Education, Inc.
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Maintenance of Body fluid Osmolality
Osmolality maintained at ~ 280 – 300 mOsm Rise in osmolality Stimulates thirst ADH release Decrease in osmolality Thirst inhibition ADH inhibition © 2013 Pearson Education, Inc.
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Regulation of Water Intake
Thirst mechanism driving force for water intake Governed by hypothalamic thirst center Hypothalamic osmoreceptors detect ECF osmolality; activated by Plasma osmolality of 1 – 2% Dry mouth Decreased blood volume or pressure Angiotensin II or baroreceptor input © 2013 Pearson Education, Inc.
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Regulation of Water Intake
Drinking water creates inhibition of thirst center Inhibitory feedback signals include Relief of dry mouth Activation of stomach and intestinal stretch receptors © 2013 Pearson Education, Inc.
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Figure 26.5 The thirst mechanism for regulating water intake.
ECF osmolality Plasma volume (5 –10%) Blood pressure Osmoreceptors in hypothalamus Saliva Granular cells in kidney Renin-angiotensin- aldosterone mechanism Dry mouth Angiotensin II Hypothalamic thirst center Sensation of thirst; person takes a drink Water moistens mouth, throat; stretches stomach, intestine Water absorbed from GI tract Initial stimulus ECF osmolality Plasma volume Physiological response Result Increases, stimulates © 2013 Pearson Education, Inc. Reduces, inhibits
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Regulation of Water Output
Obligatory water losses Insensible water loss from lungs and skin Feces Minimum daily sensible water loss of 500 ml in urine to excrete wastes Solute concentration and volume of urine a function of fluid intake, diet, and water loss via other avenues © 2013 Pearson Education, Inc.
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Regulation of Water Output: Influence of ADH
Water reabsorption in collecting ducts proportional to ADH release ADH dilute urine and volume of body fluids ADH concentrated urine; reabsorption of water volume of body fluids Hypothalamic osmoreceptors sense ECF solute concentration and regulate ADH accordingly © 2013 Pearson Education, Inc.
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Regulation of Water Output: Influence of ADH
Other factors may trigger ADH release Large changes in blood volume or pressure E.g., BP ADH release due to blood vessel baroreceptors and renin-angiotensin-aldosterone mechanism Factors lowering blood volume: intense sweating, vomiting, or diarrhea; severe blood loss; traumatic burns; and prolonged fever © 2013 Pearson Education, Inc.
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Figure 26.6 Mechanisms and consequences of ADH release.
ECF osmolality Na+ concentration in plasma Stimulates Plasma volume (5–10%), BP Osmoreceptors in hypothalamus Inhibits Negative feedback inhibits Baroreceptors in atria and large vessels Stimulates Stimulates Posterior pituitary Releases ADH Antidiuretic hormone (ADH) Targets Collecting ducts of kidneys Effects Water reabsorption Results in ECF osmolality Plasma volume Scant urine © 2013 Pearson Education, Inc.
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Disorders of Water Balance
Principal abnormalities of water balance Dehydration Hypotonic hydration Edema © 2013 Pearson Education, Inc.
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Disorders of Water Balance: Dehydration
Negative fluid balance ECF water loss due to: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, diuretic abuse, endocrine disturbances Signs and symptoms: "cottony" oral mucosa, thirst, dry flushed skin, oliguria May lead to weight loss, fever, mental confusion, hypovolemic shock, and loss of electrolytes © 2013 Pearson Education, Inc.
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Figure 26.7a Disturbances in water balance.
Slide 1 Excessive loss of H2O from ECF 1 ECF osmotic pressure rises 2 Cells lose H2O to ECF by osmosis; cells shrink 3 Consequences of dehydration. If more water than solutes is lost, cells shrink. © 2013 Pearson Education, Inc.
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Figure 26.7a Disturbances in water balance.
Slide 2 Excessive loss of H2O from ECF Excessive loss of H2O from ECF 1 Consequences of dehydration. If more water than solutes is lost, cells shrink. Consequences of dehydration. © 2013 Pearson Education, Inc.
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Figure 26.7a Disturbances in water balance.
Slide 3 Excessive loss of H2O from ECF 1 ECF osmotic pressure rises 2 Consequences of dehydration. If more water than solutes is lost, cells shrink. © 2013 Pearson Education, Inc.
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Figure 26.7a Disturbances in water balance.
Slide 4 Excessive loss of H2O from ECF 1 ECF osmotic pressure rises 2 Cells lose H2O to ECF by osmosis; cells shrink 3 Consequences of dehydration. If more water than solutes is lost, cells shrink. © 2013 Pearson Education, Inc.
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Disorders of Water Balance: Hypotonic Hydration
Cellular overhydration, or water intoxication Occurs with renal insufficiency or rapid excess water ingestion ECF osmolality hyponatremia net osmosis into tissue cells swelling of cells severe metabolic disturbances (nausea, vomiting, muscular cramping, cerebral edema) possible death Treated with hypertonic saline © 2013 Pearson Education, Inc.
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Figure 26.7b Disturbances in water balance.
Slide 1 Excessive H2O enters the ECF 1 ECF osmotic pressure falls 2 H2O moves into cells by osmosis; cells swell 3 Consequences of hypotonic hydration (water gain). If more water than solutes is gained, cells swell. © 2013 Pearson Education, Inc.
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Figure 26.7b Disturbances in water balance.
Slide 2 Excessive H2O enters the ECF 1 Consequences of hypotonic hydration (water gain). If more water than solutes is gained, cells swell. © 2013 Pearson Education, Inc.
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Figure 26.7b Disturbances in water balance.
Slide 3 Excessive H2O enters the ECF 1 ECF osmotic pressure falls 2 Consequences of hypotonic hydration (water gain). If more water than solutes is gained, cells swell. © 2013 Pearson Education, Inc.
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Figure 26.7b Disturbances in water balance.
Slide 4 Excessive H2O enters the ECF 1 ECF osmotic pressure falls 2 H2O moves into cells by osmosis; cells swell 3 Consequences of hypotonic hydration (water gain). If more water than solutes is gained, cells swell. © 2013 Pearson Education, Inc.
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Disorders of Water Balance: Edema
Atypical accumulation of IF tissue swelling (not cell swelling) Result of fluid out of blood or fluid into blood fluid out of blood caused by Increased capillary hydrostatic pressure and permeability Capillary hydrostatic pressure increased by incompetent venous valves, localized blood vessel blockage, congestive heart failure, blood volume Capillary permeability increased by ongoing inflammatory response © 2013 Pearson Education, Inc.
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fluid returning to blood result of
Edema fluid returning to blood result of Imbalance in colloid osmotic pressures, e.g., hypoproteinemia ( plasma protein levels low colloid osmotic pressure) Fluids fail to return at venous ends of capillary beds Results from protein malnutrition, liver disease, or glomerulonephritis © 2013 Pearson Education, Inc.
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Also caused by blocked (or surgically removed) lymphatic vessels
Edema Also caused by blocked (or surgically removed) lymphatic vessels Cause leaked proteins to accumulate in IF Colloid osmotic pressure of IF draws fluid from blood Increases diffusion distance for nutrients and oxygen Results in low blood pressure and severely impaired circulation © 2013 Pearson Education, Inc.
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Electrolytes are salts, acids, bases, some proteins
Electrolyte Balance Electrolytes are salts, acids, bases, some proteins Electrolyte balance usually refers only to salt balance Salts control fluid movements; provide minerals for excitability, secretory activity, membrane permeability Salts enter body by ingestion and metabolism; lost via perspiration, feces, urine, vomit © 2013 Pearson Education, Inc.
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Most abundant cation in ECF
Central Role of Sodium Most abundant cation in ECF Sodium salts in ECF contribute 280 mOsm of total 300 mOsm ECF solute concentration Only cation exerting significant osmotic pressure Controls ECF volume and water distribution Changes in Na+ levels affects plasma volume, blood pressure, and ECF and IF volumes © 2013 Pearson Education, Inc.
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Na+ leaks into cells; pumped out against its electrochemical gradient
Central Role of Sodium Na+ leaks into cells; pumped out against its electrochemical gradient Na+ moves back and forth between ECF and body secretions (e.g., digestive secretions) Renal acid-base control mechanisms are coupled to sodium ion transport © 2013 Pearson Education, Inc.
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Sodium Concentration Versus Sodium Content
Concentration of Na+ Determines osmolality of ECF; influences excitability of neurons and muscles Remains stable due to water shifts out of or into ICF Content of Na+ Total body content determines ECF volume and therefore blood pressure © 2013 Pearson Education, Inc.
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Table 26.2 Sodium Concentration and Sodium Content
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Regulation of Sodium Balance
No known receptors that monitor Na+ levels in body fluids Na+-water balance is linked to blood pressure and blood volume control mechanisms Changes in blood pressure or volume trigger neural and hormonal controls to regulate Na+ content © 2013 Pearson Education, Inc.
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Regulation of Sodium Balance: Aldosterone
Regardless of aldosterone presence 65% Na+ reabsorbed in proximal tubules; 25% reclaimed in loops of Henle Na + never secreted into filtrate Water in filtrate follows Na+ if ADH is present Na+ in urine water loss © 2013 Pearson Education, Inc.
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Aldosterone decreased urinary output; increased blood volume
By active reabsorption of remaining Na+ in distal convoluted tubule and collecting duct Also causes increased K+ secretion © 2013 Pearson Education, Inc.
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Regulation of Sodium Balance: Aldosterone
Renin-angiotensin-aldosterone mechanism main trigger for aldosterone release Granular cells of JGA secrete renin in response to Sympathetic nervous system stimulation filtrate osmolality stretch (due to blood pressure) of granular cells © 2013 Pearson Education, Inc.
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Regulation of Sodium Balance: Aldosterone
Renin catalyzes production of angiotensin II Prompts aldosterone release from adrenal cortex Na+ reabsorption by kidney tubules Aldosterone release also triggered by elevated K+ levels in ECF Aldosterone brings about its effects slowly (hours to days) © 2013 Pearson Education, Inc.
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triggers renin release, increasing angiotensin II
Figure Mechanisms and consequences of aldosterone release. K+ concentration in the ECF Body Na+ content triggers renin release, increasing angiotensin II Stimulates Adrenal cortex Releases Aldosterone Targets Kidney tubules Effects Na+ reabsorption K+ secretion Restores Homeostatic plasma levels of Na+ and K+ © 2013 Pearson Education, Inc.
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Regulation of Sodium Balance: ANP
Released by atrial cells in response to stretch ( blood pressure) Effects Decreases blood pressure and blood volume ADH, renin and aldosterone production excretion of Na+ and water Promotes vasodilation directly and also by decreasing production of angiotensin II © 2013 Pearson Education, Inc.
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Atrial natriuretic peptide Na+ and H2O reabsorption
Figure Mechanisms and consequences of ANP release. Stretch of atria of heart due to BP Releases Negative feedback Atrial natriuretic peptide (ANP) Targets JG complex of the kidney Hypothalamus and posterior pituitary Adrenal cortex Effects Effects Renin release* ADH release Aldosterone release Angiotensin II Inhibits Inhibits Collecting ducts of kidneys Vasodilation Effects Na+ and H2O reabsorption Results in Blood volume Results in Blood pressure © 2013 Pearson Education, Inc.
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Influence of other Hormones
Female sex hormones Estrogens: NaCl reabsorption (like aldosterone) H2O retention during menstrual cycles and pregnancy Progesterone: Na+ reabsorption (blocks aldosterone) Promotes Na+ and H2O loss Glucocorticoids: Na+ reabsorption and promote edema © 2013 Pearson Education, Inc.
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Cardiovascular Baroreceptors
Baroreceptors alert brain of increases in blood volume and pressure Sympathetic nervous system impulses to kidneys decline Afferent arterioles dilate GFR increases Na+ and water output increase Reduced blood volume and pressure © 2013 Pearson Education, Inc.
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Figure Mechanisms regulating sodium and water balance help maintain blood pressure homeostasis. Systemic blood pressure/volume Stretch in afferent arterioles Filtrate NaCl concentration in ascending limb of nephron loop Inhibits baroreceptors in blood vessels (+) (+) (+) Granular cells of kidneys (+) Sympathetic nervous system Release (+) Renin Systemic arterioles Catalyzes conversion Causes Angiotensinogen (from liver) Angiotensin I Vasoconstriction Results in Converting enzyme (in lungs) Peripheral resistance (+) Angiotensin II Posterior pituitary (+) (+) (+) Releases Systemic arterioles Adrenal cortex ADH (antidiuretic hormone) Causes Secretes (+) Vasoconstriction Aldosterone Collecting ducts of kidneys Results in Targets Causes Peripheral resistance Distal kidney tubules Causes H2O reabsorption Na+ (and H2O) reabsorption Results in Blood volume (+) stimulates Blood pressure Renin-angiotensin-aldosterone Mechanism Neural regulation (sympathetic nervous system effects) ADH release and effects © 2013 Pearson Education, Inc.
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Regulation of Potassium Balance
Importance of potassium Affects RMP in neurons and muscle cells (especially cardiac muscle) ECF [K+] RMP depolarization reduced excitability ECF [K+] hyperpolarization and nonresponsiveness © 2013 Pearson Education, Inc.
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Regulation of Potassium Balance
Hyperkalemia - too much K+ Hypokalemia - too little K+ Both disrupt electrical conduction in heart Sudden death © 2013 Pearson Education, Inc.
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Regulation of Potassium Balance
K+ part of body's buffer system H+ shifts in and out of cells in opposite direction of K+ to maintain cation balance, so ECF K+ levels rise with acidosis ECF K+ levels fall with alkalosis Interferes with activity of excitable cells © 2013 Pearson Education, Inc.
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Regulation of Potassium Balance
K+ balance controlled in cortical collecting ducts by regulating amount secreted into filtrate High K+ content of ECF favors principal cell secretion of K+ Kidneys have low ability to retain K+ so when levels low Principal cells reduce secretion and excretion of K+; type A intercalated cells reabsorb some K+ left in filtrate © 2013 Pearson Education, Inc.
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Influence of Plasma Potassium Concentration
Most important factor affecting K+ secretion is its concentration in ECF High K+ diet K+ content of ECF K+ entry into principal cells K+ secretion Low K+ diet or accelerated K+ loss reduces its secretion © 2013 Pearson Education, Inc.
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Regulation of Potassium Balance
Influence of aldosterone Stimulates K+ secretion (and Na+ reabsorption) by principal cells Adrenal cortical cells directly sensitive to K+ content of ECF Increased K+ in adrenal cortex causes Release of aldosterone K+ secretion Abnormal aldosterone levels severely influence K+ levels © 2013 Pearson Education, Inc.
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99% of body's calcium in bones Ca2+ in ECF important for
Regulation of Calcium 99% of body's calcium in bones Calcium phosphate salts Ca2+ in ECF important for Blood clotting Cell membrane permeability Secretory activities Neuromuscular excitability - most important © 2013 Pearson Education, Inc.
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Hypocalcemia excitability and muscle tetany
Regulation of Calcium Hypocalcemia excitability and muscle tetany Hypercalcemia inhibits neurons and muscle cells, may cause heart arrhythmias Calcium balance controlled by parathyroid hormone (PTH) from parathyroid gland Rarely deviates from normal limits © 2013 Pearson Education, Inc.
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PTH promotes increase in calcium levels by targeting
Influence of PTH PTH promotes increase in calcium levels by targeting Bones – osteoclasts break down matrix, releasing calcium and phosphate to blood Kidneys – increases calcium reabsorption; decreases phosphate ion reabsorption Small intestine – increases calcium absorption (indirectly through stimulation of kidney to activate vitamin D precursor) © 2013 Pearson Education, Inc.
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98% filtered calcium reabsorbed due to PTH
Influence of PTH 98% filtered calcium reabsorbed due to PTH If ECF calcium levels normal PTH secretion inhibited 75% of filtered phosphates reabsorbed in PCT PTH inhibits this by decreasing the Tm Phosphate reabsorption also affected by insulin (increases it) and glucagon (decreases it) © 2013 Pearson Education, Inc.
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Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.
Hypocalcemia (low blood Ca2+) PTH release from parathyroid gland Osteoclast activity in bone causes Ca2+ and PO43- release into blood Ca2+ reabsorption in kidney tubule Activation of vitamin D by kidney Ca2+ absorption from food in small intestine Ca2+ in blood Initial stimulus Physiological response Result © 2013 Pearson Education, Inc.
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Cl– is major anion in ECF
Regulation of Anions Cl– is major anion in ECF Helps maintain osmotic pressure of blood 99% of Cl– is reabsorbed under normal pH conditions When acidosis occurs, fewer chloride ions are reabsorbed Other anions have transport maximums and excesses are excreted in urine © 2013 Pearson Education, Inc.
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Normal pH of body fluids
Acid-base Balance pH affects all functional proteins and biochemical reactions, so closely regulated Normal pH of body fluids Arterial blood: pH 7.4 Venous blood and IF fluid: pH 7.35 ICF: pH 7.0 Alkalosis or alkalemia: arterial pH >7.45 Acidosis or acidemia: arterial pH <7.35 © 2013 Pearson Education, Inc.
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Most H+ produced by metabolism
Acid-base Balance Most H+ produced by metabolism Phosphorus-containing protein breakdown releases phosphoric acid into ECF Lactic acid from anaerobic respiration of glucose Fatty acids and ketone bodies from fat metabolism H+ liberated when CO2 converted to HCO3– in blood © 2013 Pearson Education, Inc.
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Concentration of hydrogen ions regulated sequentially by
Acid-base Balance Concentration of hydrogen ions regulated sequentially by Chemical buffer systems: rapid; first line of defense Brain stem respiratory centers: act within 1–3 min Renal mechanisms: most potent, but require hours to days to effect pH changes © 2013 Pearson Education, Inc.
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Acid-base Balance: Chemical Buffer Systems
Strong acids dissociate completely in water; can dramatically affect pH Weak acids dissociate partially in water; are efficient at preventing pH changes Strong bases dissociate easily in water; quickly tie up H+ Weak bases accept H+ more slowly © 2013 Pearson Education, Inc.
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completely into its ions. A weak acid such as H2CO3 does not
Figure Dissociation of strong and weak acids in water. A strong acid such as HCI dissociates completely into its ions. A weak acid such as H2CO3 does not dissociate completely. © 2013 Pearson Education, Inc.
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Chemical Buffer Systems
Chemical buffer: system of one or more compounds that act to resist pH changes when strong acid or base is added Bind H+ if pH drops; release H+ if pH rises Bicarbonate buffer system Phosphate buffer system Protein buffer system © 2013 Pearson Education, Inc.
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Bicarbonate Buffer System
Mixture of H2CO3 (weak acid) and salts of HCO3– (e.g., NaHCO3, a weak base) Buffers ICF and ECF Only important ECF buffer © 2013 Pearson Education, Inc.
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Bicarbonate Buffer System
If strong acid added: HCO3– ties up H+ and forms H2CO3 HCl + NaHCO3 H2CO3 + NaCl pH decreases only slightly, unless all available HCO3– (alkaline reserve) used up HCO3– concentration closely regulated by kidneys © 2013 Pearson Education, Inc.
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Bicarbonate Buffer System
If strong base added It causes H2CO3 to dissociate and donate H+ H+ ties up the base (e.g. OH–) NaOH + H2CO3 NaHCO3 + H2O pH rises only slightly H2CO3 supply is almost limitless (from CO2 released by respiration) and subject to respiratory controls © 2013 Pearson Education, Inc.
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Phosphate Buffer System
Action nearly identical to bicarbonate buffer Components are sodium salts of: Dihydrogen phosphate (H2PO4–), a weak acid Monohydrogen phosphate (HPO42–), a weak base Unimportant in buffering plasma Effective buffer in urine and ICF, where phosphate concentrations are high © 2013 Pearson Education, Inc.
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Protein Buffer System Intracellular proteins are most plentiful and powerful buffers; plasma proteins also important Protein molecules are amphoteric (can function as both weak acid and weak base) When pH rises, organic acid or carboxyl (COOH) groups release H+ When pH falls, NH2 groups bind H+ Hemoglobin functions as intracellular buffer © 2013 Pearson Education, Inc.
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Physiological Buffering Systems
Respiratory and renal systems Regulate amount of acid or base in body Act more slowly than chemical buffer systems Have more capacity than chemical buffer systems © 2013 Pearson Education, Inc.
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Chemical buffers cannot eliminate excess acids or bases from body
Acid-Base Balance Chemical buffers cannot eliminate excess acids or bases from body Lungs eliminate volatile carbonic acid by eliminating CO2 Kidneys eliminate nonvolatile (fixed) acids produced by cellular metabolism (phosphoric, uric, and lactic acids and ketones) to prevent metabolic acidosis Kidneys also regulate blood levels of alkaline substances; renew chemical buffers © 2013 Pearson Education, Inc.
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Respiratory Regulation of H+
Respiratory system eliminates CO2 (an acid) A reversible equilibrium exists in blood CO2 + H2O H2CO3 H+ + HCO3– During CO2 unloading reaction shifts to left (and H+ incorporated into H2O) During CO2 loading reaction shifts to right (and H+ buffered by proteins) © 2013 Pearson Education, Inc.
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Respiratory Regulation of H+
Hypercapnia activates medullary chemoreceptors Increased respiratory rate and depth Rising plasma H+ activates peripheral chemoreceptors More CO2 is removed from the blood H+ concentration is reduced © 2013 Pearson Education, Inc.
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Respiratory Regulation of H+
Alkalosis depresses respiratory center Respiratory rate and depth decrease H+ concentration increases Respiratory system impairment causes acid-base imbalances Hypoventilation respiratory acidosis Hyperventilation respiratory alkalosis © 2013 Pearson Education, Inc.
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Renal Mechanisms of Acid-Base Balance
Most important renal mechanisms Conserving (reabsorbing) or generating new HCO3– Excreting HCO3– Generating or reabsorbing one HCO3– same as losing one H+ Excreting one HCO3– same as gaining one H+ © 2013 Pearson Education, Inc.
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Renal Mechanisms of Acid-Base Balance
To reabsorb bicarbonate kidney must secrete H+ To excrete excess bicarbonate kidney must retain (not secrete) H+ © 2013 Pearson Education, Inc.
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Renal Mechanisms of Acid-base Balance
Renal regulation of acid-base balance depends on kidney's ability to secrete H+ H+ secretion occurs in PCT and collecting duct type A intercalated cells: The H+ comes from H2CO3 produced in reactions catalyzed by carbonic anhydrase inside cells As H+ secreted, Na+ reabsorbed See Steps 1 and 2 of following figure © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 1 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 H+ is secreted into the filtrate. 3a Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell 3b For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase 5 CA * 1 CA 6 Tight junction Primary active transport Transport protein 6 CO2 diffuses into the tubule cell, where it triggers further H+ secretion. 5 Secondary active transport The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 2 CO2 combines with water within the tubule cell, forming H2CO3. 1 Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell ATPase ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 3 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell ATPase 2 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 4 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 H+ is secreted into the filtrate. 3a Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell ATPase 3a 2 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 5 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 3a H+ is secreted into the filtrate. Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. 3b ATPase 3a 3b 2 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 6 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 H+ is secreted into the filtrate. 3a Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell 3b For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 7 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 3a H+ is secreted into the filtrate. Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. 3b ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase 5 CA * 1 CA Tight junction Primary active transport Transport protein 5 Secondary active transport The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 8 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 3a H+ is secreted into the filtrate. Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell 3b For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase 5 CA * 1 CA 6 Tight junction Primary active transport Transport protein 6 Secondary active transport CO2 diffuses into the tubule cell, where it triggers further H+ secretion. 5 The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Renal Mechanisms of Acid-base Balance
Rate of H+ secretion changes with ECF CO2 levels CO2 in peritubular capillary blood rate of H+ secretion System responds to both rising and falling H+ concentrations © 2013 Pearson Education, Inc.
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Bicarbonate Reabsorption
To maintain alkaline reserve kidneys must replenish bicarbonate Yet tubule cells cannot reabsorb bicarbonate Must conserve filtered bicarbonate in roundabout way © 2013 Pearson Education, Inc.
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Reabsorption of Bicarbonate
CO2 combines with water in PCT cells, forming H2CO3 H2CO3 dissociates H+ is secreted, and HCO3– shunted into capillary blood Secreted H+ unites with HCO3– to form H2CO3 in filtrate, which generates CO2 and H2O HCO3– disappears from filtrate at same rate it enters peritubular capillary blood © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 1 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 H+ is secreted into the filtrate. 3a Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell 3b For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase 5 CA * 1 CA 6 Tight junction Primary active transport Transport protein 6 CO2 diffuses into the tubule cell, where it triggers further H+ secretion. 5 Secondary active transport The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 2 CO2 combines with water within the tubule cell, forming H2CO3. 1 Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell ATPase ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 3 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell ATPase 2 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 4 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 H+ is secreted into the filtrate. 3a Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell ATPase 3a 2 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 5 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 3a H+ is secreted into the filtrate. Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. 3b ATPase 3a 3b 2 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 6 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 H+ is secreted into the filtrate. 3a Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell 3b For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase CA * 1 CA Tight junction Primary active transport Transport protein Secondary active transport CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 7 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 3a H+ is secreted into the filtrate. Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. 3b ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase 5 CA * 1 CA Tight junction Primary active transport Transport protein 5 Secondary active transport The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Primary active transport Secondary active transport
Figure Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 8 CO2 combines with water within the tubule cell, forming H2CO3. 1 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 2 3a H+ is secreted into the filtrate. Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT cell 3b For each H+ secreted, a HCO3− enters the peritubular capillary blood either via symport with Na+ or via antiport with CI−. ATPase 3a 3b 4 Secreted H+ combines with HCO3− in the filtrate, forming carbonic acid (H2CO3). HCO3− disappears from the filtrate at the same rate that HCO3− (formed within the tubule cell) enters the peritubular capillary blood. 2 4 ATPase 5 CA * 1 CA 6 Tight junction Primary active transport Transport protein 6 Secondary active transport CO2 diffuses into the tubule cell, where it triggers further H+ secretion. 5 The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. CA Carbonic anhydrase Simple diffusion © 2013 Pearson Education, Inc.
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Generating New Bicarbonate Ions
Two mechanisms in PCT and type A intercalated cells Generate new HCO3– to be added to alkaline reserve Both involve renal excretion of acid (via secretion and excretion of H+ or NH4+) © 2013 Pearson Education, Inc.
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Excretion of Buffered H+
Dietary H+ must be balanced by generating new HCO3– H+ not excreted when filtered bicarbonate reclaimed Most filtered HCO3– is "used up" before filtrate reaches the collecting duct Generating new bicarbonate counteracts acidosis from dietary H+ © 2013 Pearson Education, Inc.
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Excretion of Buffered H+
Most important urine buffer is phosphate buffer system Intercalated cells actively secrete H+ into urine, which is buffered by phosphates and excreted Generated "new" HCO3– moves into interstitial space via cotransport system, then moves passively into peritubular capillary blood © 2013 Pearson Education, Inc.
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H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−).
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 1 CO2 combines with water within the type A intercalated cell, forming H2CO3. H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 1 2 H+ is secreted into the filtrate by a H+ ATPase pump. 3a Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary For each H+ secreted, a HCO3− enters the peritubular capillary blood via an antiport carrier in a HCO3− -CI− exchange process. 3b 1 2 3a 3b (new) ATPase 4 Secreted H+ combines with HPO42− in the tubular filtrate, Forming H2PO4−. 4 Type A intercalated cell of collecting duct 5 out in urine Primary active transport Transport protein Secondary active transport The H2PO4− is excreted in the urine. 5 Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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cell of collecting duct
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 2 CO2 combines with water within the type A intercalated cell, forming H2CO3. 1 Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary 1 (new) ATPase Type A intercalated cell of collecting duct out in urine Primary active transport Transport protein Secondary active transport Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−).
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 3 CO2 combines with water within the type A intercalated cell, forming H2CO3. H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 1 2 Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary 1 2 (new) ATPase Type A intercalated cell of collecting duct out in urine Primary active transport Transport protein Secondary active transport Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−).
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 4 CO2 combines with water within the type A intercalated cell, forming H2CO3. H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 1 2 H+ is secreted into the filtrate by a H+ ATPase pump. 3a Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary 1 2 3a (new) ATPase Type A intercalated cell of collecting duct out in urine Primary active transport Transport protein Secondary active transport Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−).
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 5 CO2 combines with water within the type A intercalated cell, forming H2CO3. H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 1 2 H+ is secreted into the filtrate by a H+ ATPase pump. 3a Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary For each H+ secreted, a HCO3− enters the peritubular capillary blood via an antiport carrier in a HCO3− -CI− exchange process. 3b 1 2 3a 3b (new) ATPase Type A intercalated cell of collecting duct out in urine Primary active transport Transport protein Secondary active transport Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−).
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 6 CO2 combines with water within the type A intercalated cell, forming H2CO3. H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 1 2 H+ is secreted into the filtrate by a H+ ATPase pump. 3a Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary For each H+ secreted, a HCO3− enters the peritubular capillary blood via an antiport carrier in a HCO3− -CI− exchange process. 3b 1 2 3a 3b (new) ATPase 4 Secreted H+ combines with HPO42− in the tubular filtrate, Forming H2PO4−. 4 Type A intercalated cell of collecting duct out in urine Primary active transport Transport protein Secondary active transport Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−).
Figure New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 7 CO2 combines with water within the type A intercalated cell, forming H2CO3. H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3−). 1 2 H+ is secreted into the filtrate by a H+ ATPase pump. 3a Nucleus Filtrate in tubule lumen Tight junction Peri- tubular capillary For each H+ secreted, a HCO3− enters the peritubular capillary blood via an antiport carrier in a HCO3− -CI− exchange process. 3b 1 2 3a 3b (new) ATPase 4 Secreted H+ combines with HPO42− in the tubular filtrate, Forming H2PO4−. 4 Type A intercalated cell of collecting duct 5 out in urine Primary active transport Transport protein Secondary active transport The H2PO4− is excreted in the urine. 5 Ion channel Simple diffusion Carbonic anhydrase Facilitated diffusion © 2013 Pearson Education, Inc.
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Ammonium Ion Excretion
More important mechanism for excreting acid Involves metabolism of glutamine in PCT cells Each glutamine produces 2 NH4+ and 2 "new" HCO3– HCO3– moves to blood and NH4+ is excreted in urine Replenishes alkaline reserve of blood © 2013 Pearson Education, Inc.
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the filtrate, taking the place of H+ on a Na+ -H+ antiport carrier. 2a
Figure New HCO3– is generated via glutamine metabolism and NH4+ secretion. Slide 1 PCT cells metabolize glutamine to NH4+and HCO3−. 1 This weak acid NH4+ (ammonium) is secreted into the filtrate, taking the place of H+ on a Na+ -H+ antiport carrier. 2a For each NH4+ secreted, a bicarbonate ion (HCO3−) enters the peritubular capillary blood via a symport carrier. 2b Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT tubule cells Glutamine Glutamine Glutamine Deamination, oxidation, and acidification (+H+) 1 2a 2b (new) 3 out in urine ATPase Tight junction Primary active transport Simple diffusion The NH4+ is excreted in the urine. 3 Secondary active transport Transport protein © 2013 Pearson Education, Inc.
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Primary active transport Simple diffusion Secondary active transport
Figure New HCO3– is generated via glutamine metabolism and NH4+ secretion. Slide 2 PCT cells metabolize glutamine to NH4+and HCO3−. 1 Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT tubule cells Glutamine Glutamine Glutamine Deamination, oxidation, and acidification (+H+) 1 (new) out in urine ATPase Tight junction Primary active transport Simple diffusion Secondary active transport Transport protein © 2013 Pearson Education, Inc.
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the filtrate, taking the place of H+ on a Na+ -H+ antiport carrier. 2a
Figure New HCO3– is generated via glutamine metabolism and NH4+ secretion. Slide 3 PCT cells metabolize glutamine to NH4+and HCO3−. 1 This weak acid NH4+ (ammonium) is secreted into the filtrate, taking the place of H+ on a Na+ -H+ antiport carrier. 2a For each NH4+ secreted, a bicarbonate ion (HCO3−) enters the peritubular capillary blood via a symport carrier. 2b Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT tubule cells Glutamine Glutamine Glutamine Deamination, oxidation, and acidification (+H+) 1 2a 2b (new) out in urine ATPase Tight junction Primary active transport Simple diffusion Secondary active transport Transport protein © 2013 Pearson Education, Inc.
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the filtrate, taking the place of H+ on a Na+ -H+ antiport carrier. 2a
Figure New HCO3– is generated via glutamine metabolism and NH4+ secretion. Slide 4 PCT cells metabolize glutamine to NH4+and HCO3−. 1 This weak acid NH4+ (ammonium) is secreted into the filtrate, taking the place of H+ on a Na+ -H+ antiport carrier. 2a For each NH4+ secreted, a bicarbonate ion (HCO3−) enters the peritubular capillary blood via a symport carrier. 2b Nucleus Filtrate in tubule lumen Peri- tubular capillary PCT tubule cells Glutamine Glutamine Glutamine Deamination, oxidation, and acidification (+H+) 1 2a 2b (new) 3 out in urine ATPase Tight junction Primary active transport Simple diffusion The NH4+ is excreted in the urine. 3 Secondary active transport Transport protein © 2013 Pearson Education, Inc.
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Bicarbonate Ion Secretion
When body in alkalosis, type B intercalated cells Secrete HCO3– Reclaim H+ to acidify blood © 2013 Pearson Education, Inc.
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Bicarbonate Ion Secretion
Mechanism is opposite of bicarbonate ion reabsorption process by type A intercalated cells Even during alkalosis, nephrons and collecting ducts conserve more HCO3– than they excrete © 2013 Pearson Education, Inc.
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Abnormalities of Acid-Base Balance
All classed as respiratory or metabolic Respiratory acidosis and alkalosis Caused by failure of respiratory system to perform pH-balancing role Single most important indicator is blood PCO2 Metabolic acidosis and alkalosis All abnormalities other than those caused by PCO2 levels in blood; indicated by abnormal HCO3– levels © 2013 Pearson Education, Inc.
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Respiratory Acidosis and Alkalosis
Most important indicator of adequacy of respiratory function is PCO2 level (normally 35–45 mm Hg) PCO2 above 45 mm Hg respiratory acidosis Common cause of acid-base imbalances Due to decrease in ventilation or gas exchange CO2 accumulates in blood Characterized by falling blood pH and rising PCO2 © 2013 Pearson Education, Inc.
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Respiratory Acidosis and Alkalosis
PCO2 below 35 mm Hg respiratory alkalosis Common result of hyperventilation often due to stress or pain CO2 eliminated faster than produced © 2013 Pearson Education, Inc.
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Metabolic Acidosis and Alkalosis
Metabolic acidosis – low blood pH and HCO3– Causes Ingestion of too much alcohol ( acetic acid) Excessive loss of HCO3– (e.g., persistent diarrhea) Accumulation of lactic acid (exercise or shock), ketosis in diabetic crisis, starvation, and kidney failure © 2013 Pearson Education, Inc.
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Metabolic Acidosis and Alkalosis
Metabolic alkalosis much less common than metabolic acidosis Indicated by rising blood pH and HCO3– Causes include vomiting of acid contents of stomach or by intake of excess base (e.g., antacids) © 2013 Pearson Education, Inc.
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Effects of Acidosis and Alkalosis
Blood pH below 6.8 depression of CNS coma death Blood pH above 7.8 excitation of nervous system muscle tetany, extreme nervousness, convulsions, death often from respiratory arrest © 2013 Pearson Education, Inc.
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Respiratory and Renal Compensations
If acid-base imbalance due to malfunction of physiological buffer system, other one tries to compensate Respiratory system attempts to correct metabolic acid-base imbalances Kidneys attempt to correct respiratory acid-base imbalances © 2013 Pearson Education, Inc.
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Respiratory Compensation
Changes in respiratory rate and depth In metabolic acidosis High H+ levels stimulate respiratory centers Rate and depth of breathing elevated Blood pH is below 7.35 and HCO3– level is low As CO2 eliminated by respiratory system, PCO2 falls below normal © 2013 Pearson Education, Inc.
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Respiratory Compensation
Respiratory compensation for metabolic alkalosis revealed by: Slow, shallow breathing, allowing CO2 accumulation in blood High pH (over 7.45), elevated HCO3– levels, PCO2 above 45 mm Hg © 2013 Pearson Education, Inc.
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Renal Compensation for Respiratory Acid-Base Imbalance
Hypoventilation causes elevated PCO2 Respiratory acidosis Renal compensation indicated by high PCO2 (causes acidosis) and HCO3– levels (indicates kidneys compensating) Respiratory alkalosis exhibits low PCO2 and high pH Renal compensation is indicated by decreasing HCO3– levels © 2013 Pearson Education, Inc.
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Acid-base Imbalances Respiratory system cannot compensate for respiratory acidosis or alkalosis Renal system cannot compensate for acid-base imbalances caused by renal problems © 2013 Pearson Education, Inc.
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Developmental Aspects
Infants have proportionately more ECF than adults until about 2 years of age Problems with fluid, electrolyte, and acid-base balance are most common in infancy, reflecting Low residual lung volume High rate of fluid intake and output High metabolic rate, yielding more metabolic wastes High rate of insensible water loss Inefficiency of kidneys, especially during first month 1st month newborns risk dehydration and acidosis © 2013 Pearson Education, Inc.
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Developmental Aspects
At puberty, sexual differences in body water content arise as males develop greater muscle mass In old age, total body water often decreases Homeostatic mechanisms slow down with age Elderly may be unresponsive to thirst cues at risk for dehydration; risk of congestive heart failure and diabetes mellitus that cause fluid, electrolyte or acid-base problems © 2013 Pearson Education, Inc.
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