Evidence for a physiological role of renal sympathetic nerves in adrenergic stimulation of renin release in the rat.
Previous studies on renin release by an in vitro system of rat kidney slices, which is devoid of hemodynamic influences, have provided evidence that renin release is stimulated by a beta-adrenergic mechanism. We used this system to study effects of tyramine (an indirectly acting amine capable of displacing endogenous catecholmines from sympathetic nerve endings) on renin release. Tyramine (10(-3)M) in the presence of a monoamine oxidase inhibitor (pheniprazine, 10(-5)M) and a phosphodiesterase inhibitor (theophylline, 10(-3)M) significantly (P less than 0.01) stimulated renin release when values were compared to control observations for media containing only the inhibitors. Tyramine-induced stimulation of renin release was blocked by the beta-blocking agent, propranolol (2 X 10(-4) M), and the neural uptake blocking agent, cocaine (10(-5) M), but not by the alpha-antagonist, phentolamine (9 X 10(-4) M). These observations demonstrate a potential role for the sympathetic innervation of the juxtaglomerular apparatus on renin release.
Evidence for a physiological role of renal sympathetic nerves in adrenergic stimulation of renin release in the rat. Previous studies on renin release by an in vitro system of rat kidney slices, which is devoid of hemodynamic influences, have provided evidence that renin release is stimulated by a beta-adrenergic mechanism. We used this system to study effects of tyramine (an indirectly acting amine capable of displacing endogenous catecholmines from sympathetic nerve endings) on renin release. Tyramine (10(-3)M) in the presence of a monoamine oxidase inhibitor (pheniprazine, 10(-5)M) and a phosphodiesterase inhibitor (theophylline, 10(-3)M) significantly (P less than 0.01) stimulated renin release when values were compared to control observations for media containing only the inhibitors. Tyramine-induced stimulation of renin release was blocked by the beta-blocking agent, propranolol (2 X 10(-4) M), and the neural uptake blocking agent, cocaine (10(-5) M), but not by the alpha-antagonist, phentolamine (9 X 10(-4) M). These observations demonstrate a potential role for the sympathetic innervation of the juxtaglomerular apparatus on renin release.