BIPHASIC EFFECT OF EXTRACELLULAR [K] ON ISOPROTERENOL-STIMULATED RENIN SECRETION FROM RAT-KIDNEY SLICES

  • 1 January 1980
    • journal article
    • research article
    • Vol. 214  (3) , 541-545
Abstract
Large changes in extracellular K concentration [K], in either direction from normal, lead to depolarization of the cell and depolarization may inhibit the secretion of renin from juxtaglomerular cells. Renin secretion of rat kidney slices was examined as a function of [K]. Increases in [K] (from 4-45 or to 60 mM) 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] inhibited secretion; the combined effect of increased [K] and decreased [Na] completely blocked the stimulatory effect of isoproterenol. The Ca antagonist D-600 [methoxy verapamil] 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) inhibited basal and isoproterenol-stimulated secretion and this effect was not antagonized by D-600. Depolarization may not inhibit renin secretion but increases in intracellular [Ca] (due to 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]) may antagonize both basal and isoproterenol-stimulated renin secretion.