Circulatory responses to angiotensin in man

This report presents hemodynamic responses to the intravenous administration of synthetic angiotensin II in thirty‐nine subjects with normal and abnormal cardiovascular systems. Small doses of angiotensin produced no significant change in mean cardiac output; large doses of angiotensin consistently reduced cardiac output. Significant reductions in splanchnic and renal blood flow were produced by all doses tested. The fall in splanchnic blood flow was found to be a dose‐related phenomenon, with reductions of greater than 50 per cent of the control measurements recorded at high rates of infusion. Pretreatment with atropine lessened or prevented the reduction of cardiac output by large doses of angiotensin, but it did not alter the splanchnic‐flow responses nor prevent the reduction in renal blood flow. The regional effects were, therefore, not explained by reductions in total blood flow but by increased vascttlar resistance in these specific areas. When cardiac output is maintained, angiotensin may produce a significant augmentation of blood flow to regions other than the splanchnic and renal.