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Purified natural decapeptide angiotensin was infused intravenously at a constant rate for 32 minutes in 5 normotensive subjects. There was no significant change in the cardiac output. There were significant increases in the pulmonary artery, the pulmonary wedge, and the brachial artery pressures. There were significant increases in the systemic vascular and the total pulmonary resistances. There was no significant change in the pulmonary arteriolar resistance. The data indicate that angiotensin I produces peripheral arteriolar constriction and fail to demonstrate a concomitant pulmonary arteriolar constriction. Thus, they are consistent with an hypothesis implicating angiotensin as a causative agent in human essential hypertension.

General and Pulmonary Hemodynamic Effects of Pure Decapeptide Angiotensin in Normotensive Man