Rudin A, Granérus G, Aurell M
Scand J Urol Nephrol Suppl. 1984;79:59-62.
Three patients with Bartter's syndrome were studied under metabolic ward conditions. Renal function and the reninangiotensin system were evaluated in three different settings: before and during captopril treatment and during administration of captopril and indomethacin. Captopril induced renal vasodilation with an increase in renal plasma flow by 23%. The addition of indomethacin abolished this change. Captopril increased the release of renin and the concentration of angiotensin II in plasma decreased without being completely normalized. Indomethacin thereafter reduced plasma concentration of renin, which was, however, still higher than the control level. The plasma concentration of angiotensin II did not change significantly. In conclusion, prostaglandin synthetase inhibition annihilated the effect of captopril on renal hemodynamics and renin release.
对三名巴特综合征患者在代谢病房条件下进行了研究。在三种不同情况下评估了肾功能和肾素 - 血管紧张素系统：卡托普利治疗前、治疗期间以及卡托普利与吲哚美辛联合给药期间。卡托普利诱导肾血管舒张，肾血浆流量增加23%。加入吲哚美辛消除了这种变化。卡托普利增加了肾素释放，血浆中血管紧张素II浓度降低，但未完全恢复正常。此后吲哚美辛降低了肾素的血浆浓度，然而，该浓度仍高于对照水平。血管紧张素II的血浆浓度没有显著变化。总之，前列腺素合成酶抑制消除了卡托普利对肾血流动力学和肾素释放的影响。
