Acute hemodynamic effects of angiotensin II. Preliminary report.

Angiotensin II was given to over 200 patients during heart catheterization studies. Left to right shunts through atrial and ventricular septal defects were increased. Shunts not detected under control conditions could then be recognized. In normal subjects left atrial pressure increased about 5-10 mm. Hg, producing a secondary rise in pulmonary artery pressure. The response of the pulmonary vessels to angiotensin was usually passive. Cardiac output declined in the normal subject after angiotensin administration. Right to left shunts decreased after angiotensin administration in some patients with cyanotic congenital heart disease, thus decreasing cyanosis. This finding has possible therapeutic applications. The pulmonary arterioles of patients with pulmonary hypertension may respond to angiotensin in a different manner from those with normal pulmonary arterioles.