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[新型转换酶抑制剂盐酸地拉普利对高血压患者肾功能、肾素-血管紧张素-醛固酮系统及激肽释放酶-激肽-前列腺素系统的长期影响]

[The long-term effects of a new converting enzyme inhibitor, delapril hydrochloride, on renal function, renin-angiotensin-aldosterone system and kallikrein-kinin prostaglandin system in hypertensive patients].

作者信息

Nishiyama K, Igari T, Nanba S, Ishii M

机构信息

Department of Internal Medicine, Japanese Red Cross Medical Center, Tokyo.

出版信息

Nihon Jinzo Gakkai Shi. 1990 Jul;32(7):801-7.

PMID:2273596
Abstract

The effects of a new angiotensin converting enzyme inhibitor, delapril hydrochloride, (delapril) on renal function, and the renin-angiotensin-aldosterone and kallikrein-kinin prostaglandin systems were studied in 10 hypertensive patients. After 4 to 12 months (7.6 +/- 0.9 [SE]) of treatment with 15-60 mg/day (36 +/- 6.8) of delapril (b.i.d.), mean arterial pressure was decreased from 126 +/- 3.0 to 110 +/- 4.4 mmHg (p less than 0.01). Although renal blood flow (RBF), assessed by PAH clearance and hematocrit, was increased from 437 +/- 51 to 490 +/- 49 ml/min (p less than 0.05) and renal vascular resistance was decreased (p less than 0.05), glomerular filtration rate, measured by endogenous creatinine clearance, did not change significantly. Thus, filtration fraction was reduced (p less than 0.01). Plasma renin activity was increased from 1.5 +/- 0.3 to 4.4 +/- 1.1 ng/ml/hr (p less than 0.01). Plasma aldosterone concentration tended to decrease (p less than 0.1), and urinary aldosterone excretion showed on significant change. Although urinary kallikrein and prostaglandin E2 excretions were increased (p less than 0.05), urinary thromboxane B2 excretions was reduced (p less than 0.05). In addition, the changes in RBF were significantly correlated with those in urinary PGE2 excretion (r = 0.63, p less than 0.05). These results suggest that the antihypertensive effect of delapril is multifactorial and that the improvement of RBF seen during delapril administration in the present study may be partly due to the suppression of the renin-angiotensin-aldosterone system and the activation of kallikrein-kinin-prostaglandin system.

摘要

在10例高血压患者中研究了一种新型血管紧张素转换酶抑制剂盐酸地拉普利(地拉普利)对肾功能以及肾素 - 血管紧张素 - 醛固酮系统和激肽释放酶 - 激肽 - 前列腺素系统的影响。在用15 - 60mg/天(36±6.8)的地拉普利(每日两次)治疗4至12个月(7.6±0.9[标准误])后,平均动脉压从126±3.0降至110±4.4mmHg(p<0.01)。尽管通过对氨基马尿酸清除率和血细胞比容评估的肾血流量(RBF)从437±51增加至490±49ml/分钟(p<0.05)且肾血管阻力降低(p<0.05),但通过内生肌酐清除率测量的肾小球滤过率无显著变化。因此,滤过分数降低(p<0.01)。血浆肾素活性从1.5±0.3增加至4.4±1.1ng/ml/小时(p<0.01)。血浆醛固酮浓度有降低趋势(p<0.1),尿醛固酮排泄无显著变化。尽管尿激肽释放酶和前列腺素E2排泄增加(p<0.05),但尿血栓素B2排泄减少(p<0.05)。此外,RBF的变化与尿PGE2排泄的变化显著相关(r = 0.63,p<0.05)。这些结果表明地拉普利的降压作用是多因素的,并且在本研究中地拉普利给药期间观察到的RBF改善可能部分归因于肾素 - 血管紧张素 - 醛固酮系统的抑制和激肽释放酶 - 激肽 - 前列腺素系统的激活。

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