Summary Angiotensin II was infused into the adrenal arterial blood supply or intravenously in sheep which were either sodium replete, that is in normal sodium balance or sodium loaded, or sodium depleted by loss of parotid saliva. Aldosterone secretian was always increased in the sodium replete condition when the rate of infusion exceeded 0.1 μg./hr. intra‐arterially or 10 μg./hr. intravenously. The aldosterone response was greatly reduced when the animals were sodium loaded or sodium depleted. When sodium balance was positive, the increase of aldosterone secretion was inversely proportional to the plasma sodium concentration but it was not significantly related to the plasma potassium concentration. The inverse relation to plasma sodium did not continue into sodium depletion. When sodium balance was negative and plasma sodium concentration tended to be reduced, angiotensin infusion did not usually cause further increase of aldosterone secretion. Nephrectomy of sodium depleted animals caused aldosterone secretion to fall to basal in 8–12 hr. and restored the adrenal response to infused angiotensin II or sheep renin. Secretion rates of cortisol and corticosterone were not increased significantly by infusion of angiotensin II into the adrenal arterial blood supply. Glucocorticoid secretion was usually increased during intravenous infusion, the effect on cortisol secrection being more consistent. Systemic infusion of angiotensin II at rates which cause lartic increases of blood pressure may also cause increased release of adrenocorticotrophic hormone. It is concluded that the adrenal action of angiotensin II is primarily and predominantly on aldosterone secretion and the magnitude of this action is influenced by ambient sodium concentration and other humoral or intra‐adrenal factors operating in sodium depletion.
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Blair‐West et al. (1970) studied this question.