Central action of angiotensin and hypertension--increased central vasomotor outflow by angiotensin.

Abstract

Sympathetic nerve activities in chloralose-anesthetized dogs were recorded directly during infusions of angiotensin into vertebral artery and femoral vein. 1. With vertebral artery infusion of angiotensin arterial pressure increased to 27 ± 11.1 mmHg and pressure rising began 20 ± 6.6 seconds after starting the infusion. Intravenous infusion of the same doses of angiotensin induced arterial pres-sure rise of 10 ± 6.6 mmHg and its onset was 68 ± 29.8 seconds. 2. Rise in arterial pressure was associated with initial augmentation of nerve activity in splanchnic and renal nerves. Cardiac nerve activity was not increased. 3. During arterial pressure was maintained at a higher level, a characteristic change in nerve activity was that rhythmical discharges in renal nerve activity disappeared completely and small non-rhythmical activity occurred instead, while the large bursts of discharges in splanchnic nerve activity never disappeared. 4. The pressor response to angiotensin was inhibited by pretreatment with guanethidine, but not with atropin. The results suggest that angiotensin acts on central nervous system to increase central sympathetic outflow in splanchnic nerves, resulting in a rise in arterial pressure.