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原发性高血压患者接受依那普利两个月治疗后的全身及肾脏血流动力学变化。

Systemic and renal hemodynamic changes after two-month treatment with enalapril in patients with essential hypertension.

作者信息

Valvo E, Gammaro L, Bedogna V, Tonon M, Giorgetti P, Pica B, Antonini P, Tessitore N, Oldrizzi L, Rugiu C

机构信息

Department of Nephrology, University Hospital of Verona, Italy.

出版信息

Int J Clin Pharmacol Ther Toxicol. 1987 Dec;25(12):656-9.

PMID:2830196
Abstract

Twelve essential hypertensive patients with normal renal function were treated once daily with a new angiotensin converting enzyme inhibitor, enalapril maleate, for about two months. In all patients, the drug-induced changes in blood pressure (BP), systemic and renal hemodynamics, plasma renin activity (PRA), and urine aldosterone (UA) were evaluated. Mean arterial pressure was significantly lowered. No significant changes in cardiac index, heart rate, and stroke index were observed, while peripheral vascular resistance index was significantly decreased. Plasma and blood volumes were not significantly altered. The effects on renal hemodynamics consisted of a significant increase in renal plasma flow (RPF), a decrease in renal vascular resistance, and no change in glomerular filtration rate (GFR). UA excretion was significantly reduced during enalapril therapy. The drug was well tolerated, and no side effects were observed. In summary, enalapril is able to reduce blood pressure through a vasodilatatory effect without change in cardiac output. It increases renal blood flow with no change in glomerular filtration rate.

摘要

12例肾功能正常的原发性高血压患者每日接受一次新型血管紧张素转换酶抑制剂马来酸依那普利治疗,为期约两个月。对所有患者评估了药物引起的血压(BP)、全身及肾脏血流动力学、血浆肾素活性(PRA)和尿醛固酮(UA)的变化。平均动脉压显著降低。未观察到心脏指数、心率和每搏指数有显著变化,而外周血管阻力指数显著下降。血浆和血容量无显著改变。对肾脏血流动力学的影响包括肾血浆流量(RPF)显著增加、肾血管阻力降低以及肾小球滤过率(GFR)无变化。依那普利治疗期间UA排泄显著减少。该药物耐受性良好,未观察到副作用。总之,依那普利能够通过血管舒张作用降低血压,而心输出量无变化。它增加肾血流量,而肾小球滤过率无变化。

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引用本文的文献

1
Enalapril. A reappraisal of its pharmacology and therapeutic use in hypertension.依那普利。对其药理学及在高血压治疗中的应用的重新评估。
Drugs. 1992 Mar;43(3):346-81. doi: 10.2165/00003495-199243030-00005.