Potassium is both reabsorbed and secreted within the kidneys. Unlike water and sodium, whose plasma concentrations are regulated by varying the extent of their reabsorption, potassium is regulated by varying the extent of its secretion. In the proximal tubules, potassium is reabsorbed by moving it into tubular epithelial cells via basolateral Na+/K+ pumps (moves potassium into the cell) and by an as yet unidentified pathway that removes potassium from the filtrate. These mechanisms both increase intracellular potassium concentration, causing potassium to move through the basolateral potassium channels into the peritubular fluid. Thus, while some potassium is moved into the cell from the peritubular fluid (via the Na+/K+ pumps), the net movement of potassium is outward into the peritubular fluid. In the principal cells of the late distal tubule and collecting ducts, the direction of potassium movement is reversed. The Na+/K+ pumps on the basolateral membrane of each cell move potassium into the cell, which creates a gradient for the outward movement of potassium across the apical membrane and into the filtrate through potassium channels. Because the expression of Na+/K+ pumps is regulated by aldosterone and the Na+/K+ pumps increase the concentration of potassium within the cell, increases in aldosterone will increase the secretion of potassium into the filtrate. Decreases in pressure within the afferent arteriole and cardiac
baroreceptor will increase the secretion of
renin, which will ultimately elevate aldosterone and thereby increase potassium secretion. However, potassium can also have a direct effect on
aldosterone: high blood potassium concentrations can stimulate the release of aldosterone from the
adrenal cortex.