Acute and Chronic Beta-Receptor Blockade with Propranolol and the Cardiovascular Responses to Intravenous Sodium Nitroprusside in the Conscious Rabbit

Abstract

Sodium nitroprusside infused intravenously into conscious rabbits lowered blood pressure and raised heart rate and plasma noradrenaline. Acute beta blockade with propranolol, 2 mg/kg/hr i.v. for 2 hr, increased resting plasma noradrenaline and did not change the hypotensive effects of nitroprusside or the rise in plasma noradrenaline but attenuated the increase in heart rate. Chronic treatment with propranolol, 2 mg/kg twice daily for 3 weeks, did not modify the cardiovascular or reflex effects of nitroprusside. However, bilateral sinoaortic denervation augmented the hypotensive effect of nitroprusside and abolished both the heart rate and plasma noradrenaline responses to the vasodilator. The fall in blood pressure after nitroprusside is therefore attenuated by baroreflex mechanisms, which did not appear to be mediated by beta adrenoceptors or by withdrawal of vagal tone but could involve alpha-receptor-mediated vasoconstriction. Propranolol does not lower noradrenaline or modify the increase in noradrenaline after sodium nitroprusside.