Intravenous infusion of the angiotensin II antagonist [Sar1, Ala8]AII in conscious dogs with high-output heart failure decreased mean arterial pressure from 101 to 83 mmHg (P<0.01).
Absolute Event Rate: 83% vs 101%
p-value: p=<0.01
Dogs with experimental high-output heart failure (HOF) exhibit marked retention of salt and water secondary to hypersecretion of both renin and aldosterone. The present study was undertaken to evaluate the systemic and intrarenal arteriolar action of angiotensin II (AII) in dogs with HOF and to provide additional information about the role of AII in low-output states. The intravenous infusion of a specific AII antagonist, Sar1, Ala8AII (6 mug/kg min-1), into conscious dogs with HOF decreased the mean arterial pressure (AP) from 101 +/- 7 to 83 +/- 7 mmHg (P less than 0.01) after 45 min of infusion. Intrarenal arterial infusion of the AII antagonist (0.2 and 2.0 mug/kg min-1) into anesthetized dogs with HOF also decreased AP and produced a marked increase in renal blood flow (RBF) with no changes in either creatinine clearance or sodium excretion. Similar results were obtained during the intrarenal infusion of the antagonist into sodium-depleted dogs and dogs with thoracic vena caval constriction, but not in normal dogs. The data demonstrate an important role for AII in the regulation of AP and RBF in high- and low-output states.
Freeman et al. (Fri,) conducted a other in High-output heart failure. [Sar1, Ala8]AII (angiotensin II antagonist) vs. Baseline / normal dogs was evaluated on Mean arterial pressure (AP) (p=<0.01). Intravenous infusion of the angiotensin II antagonist [Sar1, Ala8]AII in conscious dogs with high-output heart failure decreased mean arterial pressure from 101 to 83 mmHg (P<0.01).