Failure of propranolol to inhibit the epinephrine-induced enhancement of responses to sympathetic nerve stimulation in the rat mesenteric vascular bed

PH Falckh, IS de la Lande, RE Stitzel, M Mano and RJ Head

CSIRO, Division of Human Nutrition, Adelaide, South Australia.

Experiments were designed to characterize the nature of the epinephrine- induced potentiation of responses to sympathetic nerve stimulation in the Hooded Wistar rat. The responses to sympathetic nerve stimulation were determined in the isolated perfused mesenteric vascular bed preparation before and after infusion of epinephrine (at 0.27 or 2.7 microM); at the conclusion of the experiment the content of epinephrine in the mesenteric artery was determined. The intraluminal infusion of epinephrine at both high and low concentrations potentiated the responses of the preparation to sympathetic nerve stimulation. Mesenteric artery concentrations of this catecholamine were unchanged at the lower concentration (0.27 microM), but were increased after perfusion of epinephrine at the higher concentration (2.7 microM). The beta adrenoceptor antagonist propranolol (0.5 microM) did not prevent the epinephrine-associated potentiation of responses to sympathetic nerve stimulation, nor did it influence the pressor effects of exogenous norepinephrine. The results suggest that beta adrenoceptors do not play a role in the epinephrine-induced potentiation of responses to sympathetic nerve stimulation in the rat mesenteric vascular bed preparation. This potentiation may, however, be related to a desensitization of presynaptic inhibitory alpha adrenoceptors.

Volume 253, Issue 2, pp. 432-436, 05/01/1990
Copyright © 1990 by American Society for Pharmacology and Experimental Therapeutics