MINERALOCORTICOID RECEPTORS AND 11-BETA-STEROID DEHYDROGENASE-ACTIVITY IN RENAL PRINCIPAL AND INTERCALATED CELLS

Aldosterone exerts complex effects on the cortical collecting duct (CC D): it increases Na+ and K+ transport, and it also influences H+ and H CO3 transport. Whether these latter effects represent direct action of aldosterone on intercalated cells (ICC) or are secondary to changes i n the transport of other electrolytes is unclear. Because the presence of specific receptors is the prerequisite of a direct steroid action, and mineralocorticoid receptors (MR) have not yet been demonstrated i n ICC, in this study we determined the density of MR directly in isola ted principal cells (PC) and beta-ICC. Purified populations of these t wo cell types were obtained from rabbit renal cortex by immunodissecti on and fluorescence-activated cell sorting. We found that both PC and beta-ICC contained a significant number of MR, although receptor densi ty was higher in PC than in beta-ICC (6,704 +/- 912 vs. 2,181 +/- 388 MR sites/cell; P < 0.001). 11 beta-Hydroxysteroid dehydrogenase (11 be ta-OHSD), an enzyme that is present predominantly in mineralocorticoid target cells, exhibited a distribution similar to that of MR in the t wo cell types. 11 beta-OHSD activity, determined by measuring the rate of conversion of [H-3]corticosterone to 11-dehydrocorticosterone, was 1.08 + 0.14 and 0.34 +/- 0.08 fmol.min(-1) 1,000 cells(-1) (P < 0.001 ) in intact PC and P-ICC, respectively. 11 beta-OHSD in both cell type s utilized NAD as cofactor. These results suggest that beta-ICC are po tential direct targets of aldosterone and that MR in both PC and beta- ICC are protected by 11 beta-OHSD.