Regulation of Potassium K+

Extracellular fluid potassium concentration normally is regulated precisely at about 4.2mEq/L,seldom rising or falling 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, an increase in plasma K+ can cause cardiac arrhythmias, and higher concentrations can lead to cardiac arrest or fibrillation.

Overview of renal potassium excretion 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 theTubules and (3) the rate of potassium secretion by the tubules.

Renal tubular sites of potassium reabsorption and secretion

The most important sites for regulating K+excretion are the principal cells of the late distal tubules and cortical collecting tubules. With a normal potassium intake of 100 mEq/day, the kidneys must excrete about 92 mEq/day (the remaining 8 milliequivalents are lost in the feces). About one third (31 mEq/day) of this amount of potassium is secreted into the distal and 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).

Basic feedback mechanism for control of extracellular fluid potassium concentration by aldosterone (Ald.). An increase in plasma potassium concentration stimulates aldosterone secretion which causes a marked increase in potassium excretion by the kidneys. The increased potassium excretion then reduces the extracellular fluid potassium concentration to normal.

Primary mechanisms by which high potassium intake raises potassium excretion. 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) reduce potassium secretion, whereas decreased hydrogen ion concentration (alkalosis) increases 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

An effect of chronic acidosis to inhibit proximal tubular sodium chloride and water reabsorption, which increases distal volume delivery, thereby stimulating the secretion of potassium. This effect overrides the inhibitory effect of hydrogen ions on the sodium potassiumATPase pump. Thus, chronic acidosis leads to a loss of potassium, whereas acute acidosis leads to decreased potassium excretion.

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 markedly 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 per cent of the total calcium in the plasma (5 mEq/L) exists in the ionized form, which is the form that has biological activity at cell membranes. The remainder is either bound to the plasma proteins (about 40 %) or complexed in the non-ionized form with anions such as phosphate and citrate (about10 %). 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. PTH can play a significant role in regulating phosphate concentration also.

PTH regulates plasma calcium concentration through three main effects: (1) by stimulating bone resorption; (2) by stimulating activation of vitamin D, which then increases intestinal reabsorption of calcium; and (3) by directly increasing renal tubular calcium reabsorption Compensatory responses to decreased plasma ionized calcium concentration mediated by (PTH) and vitamin D.

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

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.

Basic renal–body fluid feedback mechanism for control of blood volume, extracellular fluid volume, and arterial pressure.

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 to fill this extra capacity.

conditions in which ECF volume becomes markedly increased but blood volume remains normal or even slightly reduced: nephrotic syndrome, the glomerular capillaries leak large amounts of protein into the filtrate and the urine because of an increased permeability of the glomerulus A similar sequence of events occurs in cirrhosis of the liver as in nephrotic syndrome.