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Renal vein renin activity was measured by bioassay of plasma obtained from anesthetized dogs during renal arterial infusion of sympathomimetic amines, cyclic AMP, and other nucleotides. Renin secretion was calculated as the product of renal blood flow and the arterial-renal venous renin difference. Infusion of cyclic AMP significantly increased renin secretion, while administration of ATP, ADP, 5'AMP, and adenosine in quantities equimolar to cyclic AMP had no effect. Phentolamine, an rt-receptor antagonist, and dl- propranolol, a /3-receptor blocker, abolished the cyclic AMP-induced rise in renin secretion. Paradoxically, the increase in renin production induced by infusion of norepinephrine, a predominantly a-receptor agonist, was suppressed by propranolol administration, and the renin-stimluating effect of isoproterenol, a /3-receptor stimulator, was blocked by phentolamine administration. In addition, the d- and /-isomers of propranolol were equipotent in suppressing the isoproterenol-induced rise in renin secretion. Administration of AY-21,011, a B- receptor antagonist which lacks local anesthetic properties, also prevented the isoproterenol-induced rise in renin secretion, but lidocaine had no suppressive effect. The effects on renin secretion of cyclic AMP and sympathomimetic amines alone and in combination with adrenergic receptor antagonists were independent of changes in glomerular filtration rate, sodium excretion, urine flow, systemic blood pressure, and heart rate. The data suggest that cyclic AMP acts within the kidney as an intracellular mediator of renin secretion, and that phentolamine and propranolol suppress renin secretion at a site distal to cyclic AMP production, rather than by blockade of plasma membrane adrenergic receptors or inhibition of adenyl cyclase.

Effects of Cyclic AMP, Sympathomimetic Amines, and Adrenergic Receptor Antagonists on Renin Secretion