Freeman R H, Davis J O, Spielman W S, Lohmeier T E
Am J Physiol. 1975 Aug;229(2):474-8. doi: 10.1152/ajplegacy.1975.229.2.474.
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, Ala8]AII (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.
患有实验性高输出量心力衰竭（HOF）的犬，由于肾素和醛固酮分泌过多，会出现明显的盐和水潴留。本研究旨在评估血管紧张素II（AII）对HOF犬的全身及肾内小动脉的作用，并提供有关AII在低输出量状态中作用的更多信息。向清醒的HOF犬静脉输注特异性AII拮抗剂[Sar1，Ala8]AII（6微克/千克·分钟-1），输注45分钟后，平均动脉压（AP）从101±7降至83±7毫米汞柱（P<0.01）。向麻醉的HOF犬肾内动脉输注AII拮抗剂（0.2和2.0微克/千克·分钟-1），也会降低AP，并使肾血流量（RBF）显著增加，而肌酐清除率或钠排泄均无变化。在向缺钠犬和腔静脉狭窄犬肾内输注拮抗剂时也获得了类似结果，但正常犬未出现此情况。数据表明，AII在高输出量和低输出量状态下对AP和RBF的调节中起重要作用。
