75-80% of sodium (NaCl) in renal filtrate is reabsorbed in proximal tubules of kidneys. Aldosterone aids in actively reabsorbing remaining Na + Cl - in distal convoluted tubule/collecting tubule by increasing tubule permeability; therefore aldosterone promotes both sodium and water retention Mechanism: increase in K or decease in Na in blood plasma renin-angiotensin Mechanism stimulates adrenal cortex to release aldosterone aldosterone targeted towards the kidney tubules increase in Na reabsorption increase in K secretion restores homeostatic plasma levels of Na and K
Influences on aldosterone synthesis and release: Elevated potassium levels in ECF directly stimulates adrenal cells to secrete aldosterone Juxtaglomerular apparatus of renal tubes release renin in response to: decreased stretch (due to decrease in blood pressure) decreased filtrate osmolarity sympathetic nervous system stimulation Cardiovascular system As blood volume (and pressure) rises, the baroreceptors in the heart and in the large vessels of the neck and thorax (carotid arteries and aorta) communicate to the hypothalamus Sympathetic nervous system impulses to kidneys decrease, allowing afferent arterioles to dilate; as the glomerular filtration rate rises, sodium and water output increases (causing pressure diuresis) Reduced blood volume and pressure results
Influence of ADH Amount of water reabsorbed in the distal segments of the kidney tubules is proportional to ADH release (increase in ADH secretion = increase in water resorption) Osmoreceptors of the hypothalamus sense the ECF solute concentrations and trigger or inhibit ADH release from the pituitary Mechanism: decrease in sodium concentration in plasma (decreased osmolarity) stimulates osmoreceptors in hypothalamus stimulates posterior pituitary to release ADH ADH targeted toward distal and collecting tubules of kidney the effect is increased water resorption plasma volume increases, osmolarity decreases scant urine produced
Influence of atrial natriuretic factor (ANF) Reduces blood pressure and blood volume by inhibiting nearly all events that promote vasoconstriction and sodium and water retention
The regulatory site of potassium is in the renal tubules Influence of aldosterone Influence of plasma potassium concentrations
Regulation of Potassium Balance Potassium is the chief intracellular cation Relative intracellular-extracellular potassium concentrations directly affects a cell's resting membrane potential, therefore a slight change on either side of the membrane has profound effects (ie. on neurons and muscle fibers) Potassium is part of the body's buffer system, which resists changes in pH of body fluids; ECF potassium levels rise with acidosis (decrease pH) as potassium leave cells and fall with alkalosis (increase pH) as potassium moves into cells Potassium balance is maintained primarily by renal mechanisms Potassium reabsorption from the filtrate is constant % is lost in urine regardless of need; because potassium content of ECF is low (compared to sodium concentration), potassium balance is accomplished by changing amount of potassium secreted into the filtrate; therefore regulated by collecting tubules
Influence of Parathyroid Hormone Influence of Calcitonin
Regulation of Calcium Balance 99% of calcium found in bones as an apatite Calcium needed for blood clotting, nerve transmission, enzyme activation, etc... Calcium ion concentration is regulated by interaction of two hormones: parathyroid hormone and calcitonin Calcium ion homeostasis: effects of PTH and calcitonin PTH - released by the parathyroid cells, promotes increase in calcium levels by targeting... bones - PTH activates osteoclasts, which breakdown the matrix small intestines - PTH enhances intestinal absorption of calcium ions indirectly by stimulating the kidneys to transform vitamin D to its active form which is a necessary cofactor for calcium absorption Kidneys - PTH increases calcium reabsorption by renal tubes while simultaneously decreasing phosphate ion reabsorption Calcitonin - targets bone to encourage deposition of calcium salts and inhibits bone reabsorption (therefore an antagonist of PTH
Influence of Parathyroid Hormone Decreases plasma phosphate concentrations while increasing calcium concentrations Influence of Calcitonin Increases plasma phosphate concentration while decreasing calcium concentrations
Magnesium PTH increases plasma magnesium concentrations by causing a decrease in the amount of magnesium excreted by the kidneys Anions Chloride is indirectly increased by Aldosterone because it passively follows sodium
Respiratory acidosis Increased CO 2 =increased H + =decreased pH Hypoventilation To compensate: increase excretion of H+ or by increased reabsorption of HCO 3 - Respiratory alkalosis Decreased CO 2 =decreased H + =increased pH Hyperventilation To compensate: decreased H+ excretion or by decreased reabsorption of HCO 3 -
Three Types: Bicarbonate Buffers Phosphate Buffers Protein Buffers
Major extracellular buffering system HCO 3 - functions as a weak base while H 2 CO 3 functions as a weak acid. Example: HCl + NaHCO 3 - H 2 CO 3 + NaCl
Important in urine and intracellular buffering systems However NaH 2 PO 4 acts as the weak acid and Na 2 HPO 4 serves as the weak base. Example: HCl + Na 2 HPO 4 NaH 2 PO 4 + NaCl
Most abundant buffering system in the body including intracellular and extracellular compartments. Carboxyl groups (COOH) and amine groups (NH 3 ) act as either an acid or a base respectively.
Two Types: Respiratory Buffering System Renal Buffering System
Respiratory System Rising plasma H + causes deeper, rapid breathing which decreases CO 2 blood thereby decreasing H + ions.
Renal System To counteract acidosis, H + is secreted into the renal tubules and excreted in urine or NH 4 + is excreted rather than reabsorbed. To counteract alkalosis, bicarbonate ions are secreted into the filtrate and H + is reabsorbed.