Renin release by rat kidney slices incubated in vitro. Role of sodium and of alpha- and beta-adrenergic receptors, and effect of vincristine.

Abstract

The role of sodium concentration, of alpha- and beta-adrenergic receptors, and of a microtubular inhibtor (vincristine) on renin release was studied in rat kidney slices in vitro. Renin release was an active, linear, and temperature-dependent process. Kidneys from young rats released much more renin than those from adults. Lowering sodium concentration inhibited renin release by one-half, even when osmolality was kept constant. Isoproterenol (10(-8) to 10(-5) M) stimulated renin release significantly in a partially dose-related manner. dl-propranolol inhibited this stimulation. Significant (P less than 0.05) inhibition of renin release was induced by l-epinephrine or l-norepinephrine (10(-5) M). In the presence of an alpha-receptor blocking drug, phenoxybenzamine (10(-5) M), inhibition no longer occurred with epinephrine and stimulation was observed with l-norepinephrine. Vincristine (10(-5) M) did not affect renin release when slices from the kidneys of normal rats or adrenalectomized, sodium-depleted rats were incubated, but significantly inhibited (P less than 0.01) release that had been stimulated in vitro by isoproterenol. These results suggest to us that there may be (1) a direct or indirect (mediated through the macula densa) effect of sodium on juxtaglomerular cells, (2) an inhibitory role for alpha-adrenergic receptors on renin release, in addition to the stimulatory role of beta-receptors, (3) possible participation of microtubules in isoproterenol-stimulated renin release, and (4) an alternative mode of secretion of renin under stimulation by adrenalectomy and salt depletion.