Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity

Acutely increasing peripheral angiotensin II (ANG II) reduces the maximum r enal sympathetic nerve activity (RSNA) observed at low mean arterial blood pressures (MAPs). We postulated that this observation could be explained by the action of ANG II to acutely increase arterial blood pressure or increa se circulating arginine vasopressin (AVP). Sustained increases in MAP and i ncreases in circulating AVP have previously been shown to attenuate maximum RSNA at low MAP. In conscious rabbits pretreated with an AVP V1 receptor a ntagonist, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng.kg(-1).min(-1)) on the relationship between MAP and RSNA whe n the acute pressor action of ANG II was left unopposed with that when the acute pressor action of ANG II was opposed by a simultaneous infusion of so dium nitroprusside (SNP). Intravenous infusion of ANG II resulted in a dose -related attenuation of the maximum RSNA observed at low MAP. When the acut e pressor action of ANG II was prevented by SNP, maximum RSNA at low MAP wa s attenuated, similar to that observed when ANG II acutely increased MAP. I n contrast, intravertebral infusion of ANG II attenuated maximum RSNA at lo w MAP significantly more than when administered intravenously. The results of this study suggest that ANG II may act within the central nervous system to acutely attenuate the maximum RSNA observed at low MAP.