Abstract

Dietary sodium depletion increases electroneutral Na-Cl absorption and potassium secretion in the proximal colon of the rat. Although sodium depletion results in secondary hyperaldosteronism, the stimulation of electroneutral Na-Cl absorption is not a typical mineralocorticoid-mediated event. These studies were performed to determine whether the aldosterone or glucocorticoid receptor mediates these changes in electrolyte transport. Continuous infusion of aldosterone at 70 micrograms.100 g body wt-1.day-1 for 7 days resulted in a significant increase in net Na+ and Cl- absorption (5.5 +/- 0.8 and 5.9 +/- 1.0 mueq.h-1.cm-2, respectively). A 7-day infusion of RU 28362, a glucocorticoid receptor-specific agonist, at 70 micrograms.100 g body wt-1.day-1 similarly increased net Na+ and Cl- absorption (5.4 +/- 1.3 and 4.1 +/- 0.5 mueq.h-1.cm-2, respectively). Both aldosterone and RU 28362 produced a minimal increase in Isc (0.4 +/- 0.2 and 0.8 +/- 0.2, respectively). Administration of spironolactone prevented the stimulation of Na+ absorption induced by aldosterone but not that by RU 28362, and aldosterone but not RU 28362 stimulated active potassium secretion. These studies indicate that aldosterone mediates the stimulation of both electroneutral Na-Cl absorption and K+ secretion produced by dietary sodium depletion and that both aldosterone and glucocorticoid agonists each stimulate electroneutral Na-Cl absorption as a result of interacting with the mineralocorticoid and glucocorticoid receptors, respectively.