Renal mechanisms for control ECF Extracellular fluid volume is determined mainly by the balance between intake and output of water and salt. In most cases, salt and fluid intakes are dictated by a person’s habits rather than by physiologic control mechanisms.

The urinary excretion changes are minimal even if GFR or reabsorption changed why and how? If bl vessels of the kidneys vasodilated and GFR increases (e.g. in high fever), this ↑↑ sodium chloride in the tubule, this lead to: (1) increased tubular reabsorption of much of the extra sodium chloride filtered (glomerulotubular balance) (2) macula densa feedback, in which ↑↑ sodium chloride in the distal tubule causes afferent arteriolar constriction and return of GFR toward normal.

↑↑ sodium chloride in the distal tubule afferent arteriolar constriction return of GFR toward normal

Integrated responses to changes in sodium intake High Sodium Intake Suppresses Antinatriuretic Systems and Activates Natriuretic Systems. These mechanisms include Activation of low pressure receptor reflexes Small increases in arterial pressure, Suppression of angiotensin II formation Stimulation of natriuretic systems

Abnormal conditions that can cause large increases in blood volume and ECF volume congestive heart failure Any condition that increases vascular capacity will also cause the blood volume to increase.

Regulation of Potassium K+

ECF potassium concentration normally is regulated precisely at about 4 ECF potassium concentration normally is regulated precisely at about 4.2mEq/L seldom ↑↑ or ↓↓ more than ± 0.3 mEq/L.

-only 2 per cent in the ECF -98 % of the total body potassium is contained in the cells (ICF) -only 2 per cent in the ECF -a single meal is often as high as 50 milliequivalents, and the daily intake usually ranges between 50 and 200 mEq/day Normal potassium intake, distribution of potassium in the body fluids, and potassium output from the body.

Why precise control of (K+)is necessary? because many cell functions are very sensitive to changes in extracellular fluid potassium concentration. Increase in plasma potassium concentration of only 3 to 4 mEq/L can cause cardiac arrhythmias, and higher concentrations can lead to cardiac arrest or fibrillation.

Factors that can alter K+ distribution between the IC-and ECF Factors Shift K+ into Cells Factors Shift K+ Out of Cells (↓ ↓ EC [K+]) (↑↑ EC [K+]) ------------------ 1-Insulin 1 - Insulin deficiency (diabet mellitus) 2-Aldosterone 2 -Aldosterone deficiency(Addison’s disease) 3-B-adrenergic stimulation 3 -B-adrenergic blockade 4-Alkalosis 4- Acidosis 5--Cell lysis 6-Strenuous exercise 7- Increased ECF osmolarity

Potassium excretion is determined by: (1) the rate of potassium filtration (GFR multiplied by the plasma potassium concentration), (2) the rate of potassium reabsorption by the tubules and (3) the rate of potassium secretion by the tubules.

Renal tubular sites of potassium reabsorption and secretion Potassium is reabsorbed in the proximal tubule and in the ascending loop of Henle only about 8 % of the filtered load is delivered to the distal tubule. Secretion of potassium into the late distal tubules and collecting ducts adds to the amount delivered, so that the daily excretion is about 12% of the potassium filtered at the glomerular capillaries. The percentages indicate how much of the filtered load is reabsorbed or secreted into the different tubular segments. Renal tubular sites of potassium reabsorption and secretion

The most important sites for regulating potassium excretion are the principal cells of the late distal tubules and cortical collecting tubules.

Factors that influence secretion The most important factors that stimulate potassium secretion by the principal cells include (1) increased ECF potassium concentration, (2) increased aldosterone, (3) increased tubular flow rate. One factor that decreases potassium secretion is increased hydrogen ion concentration(acidosis).

increased plasma potassium concentration directly raises potassium secretion by the cortical collecting tubules and indirectly increases potassium secretion by raising plasma aldosterone concentration.

- acute increases in hydrogen ion concentration of the ECF(acidosis) ↓↓ potassium secretion, - decreased hydrogen ion concentration (alkalosis) ↑↑ potassium secretion. The primary mechanism by which increased hydrogen ion concentration inhibits potassium secretion is by reducing the activity of the sodium-potassium ATPase pump This in turn decreases intracellular potassium concentration and subsequent passive diffusion of potassium across the luminal membrane into the tubule.

Renal calcium excretion Extracellular fluid calcium ion concentration normal level, 2.4 mEq/L. When calcium ion concentration falls to low levels (hypocalcemia), the excitability of nerve and muscle cells increases and can in extreme cases result in hypocalcemic tetany. This is characterized by spastic skeletal muscle contractions. Hypercalcemia (increased calcium concentration) depresses neuromuscular excitability and can lead to cardiac arrhythmias.

-About 50 % of the total calcium in the plasma (5 mEq/L) in the ionized form (has biological activity at cell membranes). -About 40% bound to the plasma proteins. -About10 % complexed in the non-ionized form with anions such as phosphate and citrate .

Changes in plasma hydrogen ion concentration can influence the degree of calcium binding to plasma proteins. With acidosis, less calcium is bound to the plasma proteins. Conversely, in alkalosis, a greater amount of calcium is bound to the plasma proteins. Therefore, patients with alkalosis are more susceptible to hypocalcemic tetany.

One of the most important regulators of bone uptake and release of calcium is PTH. When ECF calcium concentration falls below normal, the parathyroid glands are directly stimulated by the low calcium levels to promote increased secretion of PTH.

Factors that alter renal calcium excretion ↓ PTH ↑ (PTH) ↑ ECF volume ↓ ECF volume ↑ Blood pressure ↓ Blood pressure ↓ Plasma phosphate ↑Plasma phosphate Metabolic alkalosis Metabolic acidosis Vitamin D3