Pariente E A, Bataille C, Bercoff E, Lebrec D
Gastroenterology. 1985 May;88(5 Pt 1):1255-9. doi: 10.1016/s0016-5085(85)80088-3.
The reduction of angiotensin II production by captopril--an angiotensin-converting enzyme inhibitor--could suppress hyperaldosteronism without impairment of renal function and could thereby be useful in the treatment of ascites in patients with cirrhosis. Systemic and renal hemodynamics and renal function were studied in 6 nonazotemic patients with cirrhosis and ascites with a low-sodium diet before and after oral administration of 25 mg of captopril. Cardiac output and renal blood flow did not change significantly after administration of captopril, whereas mean arterial pressure significantly decreased. Systemic and renal vascular resistances were significantly reduced. There was a statistically significant reduction of glomerular filtration rate, filtration fraction, and urinary output. Plasma renin activity significantly increased in all patients after administration of captopril. A statistically significant correlation was found between the decrease in mean arterial pressure and the reduction of glomerular filtration, but no relationship was found between basal values of plasma renin activity and the other observed variations. We concluded that captopril mainly induces hypotension due to an increase in renal vasodilatation in ascitic patients with cirrhosis.
卡托普利（一种血管紧张素转换酶抑制剂）减少血管紧张素II的生成，可在不损害肾功能的情况下抑制醛固酮增多症，从而可能有助于治疗肝硬化患者的腹水。在6例非氮质血症肝硬化腹水患者中，在口服25毫克卡托普利前后，采用低钠饮食，研究了全身和肾脏血流动力学及肾功能。服用卡托普利后，心输出量和肾血流量无明显变化，而平均动脉压显著降低。全身和肾血管阻力显著降低。肾小球滤过率、滤过分数和尿量有统计学意义的降低。服用卡托普利后，所有患者的血浆肾素活性均显著增加。平均动脉压下降与肾小球滤过率降低之间存在统计学意义的相关性，但血浆肾素活性的基础值与其他观察到的变化之间未发现相关性。我们得出结论，卡托普利主要通过增加肝硬化腹水患者的肾血管舒张来诱发低血压。
