An analysis of central adrenoceptors for control of cardiovascular function

Abstract

1 In dogs anaesthetized with pentobarbitone sodium, bradycardia with hypotension occurred on intracerebroventricular (i.c.v.) injection of noradrenaline (50–200 μg) or phenylephrine (100–400 μg), but tachycardia with hypotension occurred on i.c.v. injection of isoprenaline (100–200 μg). 2 These cardiovascular responses were central effects, and from the results obtained after bilateral vagotomy, removal of both stellate ganglia and transection of the upper cervical cord, it was evident that the efferent nervous pathway for all these effects was the sympathetic nervous system. 3 An i.c.v. injection of the α-adrenoceptor blocking agent phenoxybenzamine (10 mg) blocked the bradycardia and hypotension produced by noradrenaline or phenylephrine, and an i.c.v. injection of a β-adrenoceptor blocking agent, either propranolol (2 mg) or N-isopropyl-p-nitrophenyl-ethanolamine (INPEA) (10 mg), blocked the tachycardia and hypotension produced by isoprenaline. 4 The cardiovascular effects produced by i.c.v. injection of the three sympathomimetic amines could be reproduced in cross-circulation experiments in the recipient dog when the amines were injected into its head circulation, and the effects of noradrenaline and phenylephrine, but not those of isoprenaline, were abolished by the α-adrenoceptor blocking agent yohimbine (1 mg/kg) injected intravenously into the donor dog. 5 It is concluded that the central α-adrenoceptors are concerned with bradycardia and the central β-adrenoceptors with tachycardia, but that both receptors are concerned with hypotension.