Modification of responses to sympathetic nerve stimulation by the renin-angiotensin system in rats

1 Angiotensin I (AI) and AII elicited a dose-dependent potentiation of contractions by rat vas deferens produced by low frequency nerve stimulation without enhancing the contraction produced by exogenous noradrenaline. The AII-induced presynaptic potentiation was blocked by the specific antagonist cysteine(8)-AII.2 The vasoconstrictor response to periarterial stimulation of rat isolated perfused kidney was potentiated by AII and there was a lesser enhancement of the effect of exogenous noradrenaline.3 The response to stimulation of complete sympathetic outflow from the spinal cord to blood vessels in the pithed rat was enhanced by angiotensin or vasopressin in direct proportion to the increase in prestimulus muscular tone. The blood pressure in the pithed rats is primarily maintained by the renin-angiotensin system since the converting-enzyme inhibitor (SQ-20881) or bilateral nephrectomy caused further substantial lowering of systemic blood pressure after spinal cord destruction and after treatment with curare and atropine.