Facilitation by beta-adrenoreceptors of stimulation-induced vasoconstriction in pithed spontaneously hypertensive rats.

Abstract

In pithed bilateral adrenal demedullated spontaneously hypertensive rats, slow i.v. infusion of adrenaline (500 ng/min) significantly increased pressor responses to the electrical stimulation of the entire sympathetic outflow, but had little effect on pressor responses induced by bolus injections of noradrenaline. After pretreatment with timolol (1 mg/kg, i.v., 30 min) adrenaline infusion enhanced noradrenaline-induced pressor effects, but not stimulation-induced responses. Salbutamol (50-500 ng/min, i.v.) and procaterol (2.5 ng/min, i.v.) infusions significantly potentiated stimulation-induced pressor effects without affecting noradrenaline-induced responses. Higher rates of salbutamol (5 micrograms/min, i.v.) and procaterol (25 ng/min, i.v.) infusion significantly depressed noradrenaline-induced pressor effects and attenuated those induced by sympathetic nerve stimulation. It is concluded that the potentiation of stimulation-induced pressor responses by adrenaline salbutamol and procaterol, involves a beta-adrenoreceptor mediated facilitation of sympathetic neurotransmission.