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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.

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