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伊拉地平与卡托普利联合应用对高血压患者肾功能的影响

Combined actions of isradipine and captopril on renal function in hypertension.

作者信息

Krusell L R, Sihm I, Jespersen L T, Thomsen K, Pedersen E B, Pedersen O L

机构信息

Department of Internal Medicine and Cardiology I, Aarhus Amtssygehus, Denmark.

出版信息

J Hum Hypertens. 1992 Oct;6(5):401-7.

PMID:1464898
Abstract

The object of this study was to test the hypothesis that the natriuretic and uricosuric effect of calcium-entry blockers could be mediated through antagonism of angiotensin II dependent intrarenal mechanisms. The antihypertensive efficacy, haemodynamic and excretional effects of superimposed calcium blockade with isradipine were investigated in seven hypertensives with unsatisfactorally controlled blood pressure with captopril 50 mg twice daily. Glomerular filtration rate (GFR) and renal plasma flow (RPF), clearances (C) of sodium (Na), potassium (K), uric acid (UA) and lithium (Li), were measured before and after a low-dose bolus of isradipine, i.v. Subsequently, measurements were repeated during constant i.v. infusion of a higher dose with definite systemic haemodynamic effects. After 4 months of combined treatment with isradipine and captopril renal investigations were carried out again. The low isradipine dose induced a slight but statistically significant increment in CNa (22% +/- 28) and heart rate (4% +/- 4), whereas no other variables changed significantly. Infusion of the high isradipine dose caused a pronounced fall in renal vascular resistance (27% +/- 14), systolic (8% +/- 2) and diastolic blood pressure (17% +/- 5). RPF increased significantly (15% +/- 18) whereas no changes were noted in GFR, filtration fraction and urinary albumin excretion rate. In spite of the pronounced fall in BP during the high dose infusion, significant increments in natriuresis (91% +/- 63) and diuresis (41% +/- 27) were induced. The natriuresis was caused by a proximal tubular action as indicated by increased CLi and CLi/GFR.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究的目的是检验以下假设

钙通道阻滞剂的利钠和促尿酸尿作用可能通过拮抗血管紧张素II依赖性肾内机制来介导。在7名使用卡托普利(每日两次,每次50mg)血压控制不佳的高血压患者中,研究了叠加使用伊拉地平进行钙阻滞的降压疗效、血流动力学和排泄效应。在静脉注射小剂量伊拉地平前后,测量肾小球滤过率(GFR)、肾血浆流量(RPF)、钠(Na)、钾(K)、尿酸(UA)和锂(Li)的清除率(C)。随后,在持续静脉输注具有明确全身血流动力学效应的较高剂量期间重复测量。在伊拉地平和卡托普利联合治疗4个月后,再次进行肾脏检查。低剂量伊拉地平使CNa轻微但有统计学意义地增加(22%±28),心率增加(4%±4),而其他变量无显著变化。输注高剂量伊拉地平导致肾血管阻力显著下降(27%±14),收缩压(8%±2)和舒张压(17%±5)下降。RPF显著增加(15%±18),而GFR、滤过分数和尿白蛋白排泄率无变化。尽管在高剂量输注期间血压显著下降,但仍诱导了显著的利钠增加(91%±63)和利尿增加(41%±27)。如CLi和CLi/GFR增加所示,利钠是由近端肾小管作用引起的。(摘要截短于250字)

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