Sodium, Potassium, and Aldosterone

Most of the sodium and potassium in the initial glomerular filtrate is reabsorbed by the proxi­mal tubule and the loop of Henle. However, the collecting duct is also capable of sodium and potassium transport, and it is here that the final adjustments are made in the regulation of sodium and potassium balance.

Aldosterone acts on principal cells of the collecting ducts to promote their reabsorption of sodium when sodium must be retained to maintain sodium balance. The regulation of aldosterone secretion from the adrenal cortex relative to sodium balance is via the renin­angiotensin system. When sodium must be retained (such as with a low-salt diet or after loss of extracellular fluid with sodium), the renin-angiotensin system is activated, and angiotensin ii stimulates cells of the adrenal cortex to secrete aldosterone.

The concentration of potassium in plasma and other extracellular fluids also regulates aldosterone secretion. increases in potassium concentration directly stimulate cells of the adrenal cortex to secrete aldosterone. Aldoste­rone promotes potassium secretion by principal cells, and this tends to increase the urinary loss of potassium. The increased loss of potassium in the urine reduces plasma potassium, and thus potassium plasma concentration and potassium balance are maintained. Most potas­sium in excreted urine reaches the tubular fluid by tubular secretion in the collecting duct.

Unregulated secretion of aldosterone by adrenal tumors can cause significant reduc­tions in plasma potassium concentrations, and these can threaten life. Such individuals may also have moderate degrees of sodium retention and increases in ECF volume, but this is usually not as severe as the changes in plasma potassium. The more moderate changes in sodium balance are because sodium transport by other nephron seg­ments is regulated by other factors that can counterbalance the sodium-retaining effects of aldosterone.