Biphasic effect of extracellular [K] on isoproterenol-stimulated renin secretion from rat kidney slices

PC Churchill and MC Churchill

It is known that large changes in extracellular K concentration [K], in either direction from normal, lead to depolarization of the cell and it has been suggested that depolarization inhibits the secretion of renin from juxtaglomerular cells. In the present experiments, renin secretion of rat kidney slices was examined as a function of [K]. Increases in [k] (from 4-45 or to 60mM) inhibited basal and isoproterenol-stimulated renin secretion, independently of changes in [Na], [Cl] and osmolality. At 4, 45 and 60 mM K, reductions in extracellular [Na] also inhibited secretion; the combined effect of isoproterenol. The Ca antagonist D- 600 antagonized the inhibitory effects of high [K], restoring both the basal and the isoproterenol-stimulated secretory rates to normal values. Decreasing [K] (from 2.5-1.0 mM) also inhibited basal and isoproterenol-stimulated secretion, and this effect was not antagonized by D-600. On the basis of the known actions of D-600 and the present observations, it is suggested that depolarization per se does not inhibit renin secretion but that increases in intracellular [Ca] (resulting from depolarization-induced Ca influx in the presence of high [K] or from changes in the rate of Na-Ca exchange in the presence of low [K]) antagonize both basal and isoproterenol-stimulated renin secretion.

Volume 214, Issue 3, pp. 541-545, 09/01/1980
Copyright © 1980 by American Society for Pharmacology and Experimental Therapeutics