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.
Role of central angiotensin II receptors in cold-induced hypertension
