ANGIOTENSIN-II MODULATES ARTERIAL BAROREFLEX FUNCTION VIA A CENTRAL ALPHA(1)-ADRENOCEPTOR MECHANISM IN RABBITS

To test the hypothesis that angiotensin II (ANG II) modulates arterial baroreflex function via a central alpha(1)-adrenoceptor mechanism, we examined the effects of intravertebral infusion of ANG II on barorefl ex function curves before and after intravertebral administration of t he alpha(1)-adrenoreceptor antagonist prazosin. Rabbits were chronical ly instrumented with subclavian and vertebral arterial catheters, veno us catheters, and aortic and vena caval occluders. Baroreflex curves w ere obtained by relating heart rate (HR) to mean arterial pressure dur ing increases and decreases in arterial pressure. Intravertebral infus ions of ANG II (5, 10, and 20 ng . kg(-1). min(-1)) produced a dose-de pendent shift of the midrange of the curve toward higher pressures (64 +/- 1 to 68 +/- 1, 76 +/- 1, and 85 +/- 2 mmHg, respectively). Pretre atment with prazosin (10 mu g/kg) via the vertebral artery markedly re duced the shift in the baroreflex curve induced by the highest dose of ANG II (64 +/- 2 to 70 +/- 2 mmHg). These data suggest that ANG II re sets the operating point of the HR baroreflex curve to a higher blood pressure and that this effect is mediated via a central alpha(1) mecha nism. When the effects of vertebral ANG II on the baroreflex control o f renal sympathetic nerve activity (RSNA) were examined, intravertebra l administration of ANG II, while reducing the gain and the maximum RS NA, did not reset the RSNA baroreflex curve. These data suggest that A NG II acutely resets the HR baroreflex but not the RSNA baroreflex and that the resetting involves an alpha(1)-adrenergic mechanism.