The role of endogenous angiotensin II (ANG II) at the level of the rostral (RVLM) and caudal ventrolateral medulla (CVLM) in the control of sympathetic baroreflex function was investigated in urethan-anesthetized rabbits. The baroreflex relationship between mean arterial pressure and integrated renal sympathetic nerve activity (RSNA) was compared before and during microinfusion of saralasin, an ANG II receptor antagonist into RVLM or CVLM. The infusion of saralasin (20 pmol/min) into RVLM reduced the upper plateau, the range, and the range-dependent gain of the baroreflex, as well as the resting level of RSNA. The infusion of saralasin into CVLM augmented the upper plateau, the reflex range, and the range-dependent gain, whereas it did not alter the resting level of RSNA or mean arterial pressure. These results suggest that 1) the ANG II networks in RVLM are tonically active, influencing the resting level of the sympathetic outflow and facilitating the sympathetic baroreflex function, and 2) the ANG II networks in CVLM do not significantly influence the sympathetic activity in the resting state but exert an inhibitory effect on the baroreflex response when arterial pressure falls below the resting level.

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1. Renal and cardiac sympathetic baroreflex functions were studied in sodium pentobarbitone anaesthetized rabbits given succinylcholine, during constant artificial ventilation with air and with hypoxic gas mixtures. Mean arterial pressure (MAP) was raised and lowered between values of 40 and 140 mm Hg by means of aortic and vena caval periovascular balloons and integrated sympathetic nerve activity (SNA) was recordered. 2. The relationship between MAP and SNA was sigmoid, with upper and lower plateau levels. The curves were defined by calculating median blood pressure, SNA Range and reflex gain. In both renal and cardiac sympathetics section of the carotid sinus and aortic nerves completely abolished the MAP-related changes in SNA. 3. The renal baroreflex curves were reset from control levels during hypoxia. Median blood pressure increased, as did SNA Range and gain. These effects were due to central interactions between arterial baroreceptor, arterial chemoreceptor and vagal afferent activity. 4. The cardiac sympathetic baroreflex curves were shifted in the opposite direction from control with reduction in median blood pressure, SNA Range and reflex gain. These changes were due to chemoreceptor-arterial baroreceptor interactions. 5. Arterial hypoxia thus evokes a differentiated pattern of baroreflex resetting in the renal and cardiac sympathetic montoneuron pools with differing changes in neural response range and sensitivity to arterial pressure changes.

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