Renal blockade to angiotensin II in acute and chronic sodium-retaining states.

Acute thoracic inferior vena cava constriction results in alterations in renal hemodynamics which may explain the characteristic antinatriuretic response. Since adrenalvein-aldosterone secretion is increased within 30 minutes of acute caval constriction and elevated plasma-renin activity is found in the chronic caval dog, we sought to determine whether the renal hemodynamic alterations observed in acute caval constriction are due to the intrarenal action of angiotensin II. The renal response to acute caval constriction in dogs receiving unilateral renal arterial infusion of a specific competitive antagonist of angiotensin II, 1-sarcosine-8-alanine-agiotensin II, was studied. Effective blockade did not alter the renal hemodynamic or antinatriuretic response to acute caval constriction. As a model of chronic sodium retention, dogs with chronic congestive heart failure produced by tricuspid insufficiency and pulmonary stenosis were similarly studied. Effective renal blockade to antiotensin II did not affect renal hemodynamics or urinary sodium excretion. The renal hemodynamic and antinatriuretic responses to acute caval constriction and chronic congestive heart failure are not dependent on the intrarenal action of angiotensin II.