Schroeder E T, Anderson G H, Goldman S H, Streeten D H
Kidney Int. 1976 Jun;9(6):511-9. doi: 10.1038/ki.1976.65.
1-Sar-8-ala angiotensin II (saralasin) was infused intravenously in graded doses of from 0.1 to 10 mug/kg/min to five patients with cirrhosis and ascites after three days of restricted sodium intake. In each patient blockade of AII by saralasin produced a marked fall in blood pressure, a rise in plasma renin activity (PRA) and plasma renin concentration (PRC) and, in four of the five, a fall in plasma aldosterone (PA). The rise in PRA and PRC correlated poorly with changes in blood pressure. The effects of saralasin rapidly reversed after cessation of the infusion. Plasma volume was normal or high in each case. Three patients were mildly hypotensive in the control state, and all five were resistant to the pressor effect of infused AII. After three days of salt loading, the above effects of saralasin were diminished but not abolished. In four normal subjects, after salt depletion, saralasin infusion induced qualitatively similar but much smaller changes in blood pressure, PRA and PRC. In two cirrhotic patients without ascites, after salt depletion, saralasin infusion caused a rise in blood pressure with no significant changes in PRA, PRC or PA. These results provide evidence that in patients with cirrhosis and ascites circulating AII is active in support of blood pressure, in direct suppression of renal renin release, and in stimulation of aldosterone release.
在五名肝硬化腹水患者限制钠摄入三天后，以0.1至10微克/千克/分钟的递增剂量静脉输注1- Sar - 8 - ala血管紧张素II（沙拉新）。在每名患者中，沙拉新对血管紧张素II的阻断导致血压显著下降、血浆肾素活性（PRA）和血浆肾素浓度（PRC）升高，并且在五名患者中的四名患者中，血浆醛固酮（PA）下降。PRA和PRC的升高与血压变化的相关性较差。输注停止后，沙拉新的作用迅速逆转。每种情况下血浆容量均正常或偏高。三名患者在对照状态下轻度低血压，所有五名患者对输注的血管紧张素II的升压作用均有抵抗。在盐负荷三天后，沙拉新的上述作用减弱但未消除。在四名正常受试者盐耗竭后，输注沙拉新引起血压、PRA和PRC发生定性相似但程度小得多的变化。在两名无腹水的肝硬化患者盐耗竭后，输注沙拉新导致血压升高，而PRA、PRC或PA无显著变化。这些结果证明，在肝硬化腹水患者中，循环中的血管紧张素II在维持血压、直接抑制肾素释放以及刺激醛固酮释放方面发挥作用。
