作者: Erin J Whalen , Alan Kim Johnson , Stephen J Lewis
DOI: 10.1016/S0014-2999(98)00852-8
关键词: Sympathetic nervous system 、 Chlorisondamine 、 Propranolol 、 Nitrovasodilator 、 Norepinephrine secretion 、 Internal medicine 、 Baroreceptor 、 Catecholamine 、 Endocrinology 、 Vasodilation 、 Chemistry
摘要: The aims of this study were (1) to characterize the hemodynamic mechanisms underlying hypotensive effects pituitary adenylate cyclase activating polypeptide-27 (PACAP-27 0.1-2.0 nmol/kg, i.v.) in pentobarbital-anesthetized rats, and (2) determine roles autonomic nervous system, adrenal catecholamines endothelium-derived nitric oxide (NO) expression PACAP-27-mediated on function. PACAP-27 produced dose-dependent decreases mean arterial blood pressure hindquarter mesenteric vascular resistances saline-treated rats. also pronounced falls rats treated with ganglion blocker, chlorisondamine (5 mg/kg, i.v.). vasodilator actions not attenuated by beta-adrenoceptor antagonist, propranolol (1 i.v.), or NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME 50 micromol/kg, increases heart rate whereas response nitrovasodilator, sodium nitroprusside (10 microg/kg, was associated a minimal tachycardia. PACAP-27-induced tachycardia unaffected chlorisondamine, but virtually abolished propranolol. These results suggest that are due microcirculation rather than release vasodilation may involve NO. produces directly releasing norepinephrine from cardiac sympathetic nerve terminals direct baroreceptor reflex-mediated activity.