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Direct Effect of Beta-Adrenergic Stimulation on Renin Release by the Rat Kidney Slice In Vitro

Controversy exists regarding the mechanism by which catecholamines stimulate rennin secretion in vivo. A sensitive rat kidney slice system was utilized to study the direct effects of adrenergic agonists and antagonists on renin release in vitro. Catecholamines were protected from degradation by the addition of ascorbic acid to the incubation medium. Significant dose-related stimulation of renin release was observed with epinephrine and norepinephrine in concentrations from 1.5 x 10−9 to 1.5 x 10−7M and with isoproterenol in concentrations from 2 x 10−9 to 2 x 10−7M. No significant stimulation was seen with 10−10M concentrations of the three agents. Methoxamine (10−6M) stimulated renin release significantly (P < 0.01). The stimulation observed with epinephrine, norepinephrine, or isoproterenol was blocked by d, l- and l-propranolol (2 x 10−4M) but not by d-propranolol (2 x 10−4M) or phentolamine (9 x 10−4M). Methoxamine-induced stimulation was abolished by d, l-propranolol but not by phentolamine. These data indicate that the in vitro kidney slice system is responsive to physiological concentrations of catecholamines when they are protected from degradation. The results further demonstrate a direct stimulatory role for β-adrenergic agents on renin release and suggest that α-adrenergic effects seen in vivo are mediated indirectly by hemodynamic, vascular, or functional changes in the kidney.