Stanek B, Renner F, Sedlmayer A, Silberbauer K
2nd Department of Internal Medicine, University of Vienna, Austria.
Eur J Clin Pharmacol. 1987;33(3):249-54. doi: 10.1007/BF00637557.
In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction. Captopril caused an increase in plasma renin activity (p less than 0.005) and a decrease in plasma aldosterone (p less than 0.025) from an elevated baseline, and a moderate drop in systolic (p less than 0.025) and diastolic (p less than 0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r = -0.66, p less than 0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r = 0.49, p less than 0.05 for systolic and r = 0.71, p less than 0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels. The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.
在肝硬化患者中，神经体液血管收缩系统被激活以代偿循环障碍。为了更详细地研究肾素 - 血管紧张素 - 醛固酮系统，在适度限制钠摄入后，用卡托普利抑制了15例晚期肝病患者的血管紧张素转换酶。卡托普利使血浆肾素活性从升高的基线水平上升（p<0.005），血浆醛固酮下降（p<0.025），收缩压（p<0.025）和舒张压（p<0.05）适度下降。卡托普利后的高肾素血症与当时的血浆钠水平呈负相关（r = -0.66，p<0.01），收缩压和舒张压的变化均与基线血浆肾素活性相关（收缩压r = 0.49，p<0.05；舒张压r = 0.71，p<0.01）。心率、刺激后的血浆去甲肾上腺素和血管加压素水平均无变化。数据表明，在这些肝硬化患者中，肾素 - 血管紧张素 - 醛固酮系统的反应性仍然完好，尽管其发生在较高水平。这些数据证实了肾素 - 血管紧张素 - 醛固酮系统在肝硬化患者动脉血压调节中的重要性。
