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硝苯地平在原发性高血压中的降压和利钠作用。肾激肽释放酶-激肽-前列腺素系统及肾素-血管紧张素-醛固酮系统的作用

Hypotensive and natriuretic effects of nifedipine in essential hypertension. Role of renal kallikrein-kinin-prostaglandin and renin-angiotensin-aldosterone systems.

作者信息

Tsunoda K, Abe K, Omata K, Kudo K, Sato M, Kohzuki M, Tanno M, Seino M, Yasujima M, Yoshinaga K

出版信息

J Clin Hypertens. 1986 Sep;2(3):263-70.

PMID:3640807
Abstract

To assess the role of renal kallikrein-kinin-prostaglandin and renin-angiotensin-aldosterone systems in the diuretic and natriuretic actions of nifedipine, a calcium-channel blocker, 20 mg of nifedipine was administered orally to 15 patients with essential hypertension. Nifedipine promptly induced a hypotensive effect and an increase in pulse rate. Urine volume, urinary sodium excretion, and creatinine clearance were significantly increased after the administration of nifedipine by 63.5%, 48.5% and 12.4%, respectively. Urinary excretion of kallikrein and prostaglandin E were also significantly increased after the administration of nifedipine by 29.4% and 50.0%, respectively. The change in urinary kallikrein excretion was significantly correlated with that in urine volume (r = 0.70, p less than 0.01) or that in urinary sodium excretion (r = 0.86, p less than 0.01). In addition, the change in urinary prostaglandin E excretion was also significantly correlated with that in urine volume (r = 0.72, p less than 0.01) or that in urinary sodium excretion (r = 0.53, p less than 0.05). Plasma aldosterone concentration did not change despite of the marked increase in plasma renin activity, and plasma aldosterone concentration/plasma renin activity ratio decreased after the administration of nifedipine. These results suggest that the augmented renal kallikrein-kinin-prostaglandin system and the suppressed secretion of aldosterone may be associated with the diuretic and natiuretic action of nifedipine and may contribute to the reduction in blood pressure that is caused mainly by its vasodilatory action.

摘要

为评估肾激肽释放酶 - 激肽 - 前列腺素系统及肾素 - 血管紧张素 - 醛固酮系统在钙通道阻滞剂硝苯地平的利尿和利钠作用中的角色,对15例原发性高血压患者口服20毫克硝苯地平。硝苯地平迅速产生降压作用并使心率加快。服用硝苯地平后,尿量、尿钠排泄量和肌酐清除率分别显著增加了63.5%、48.5%和12.4%。服用硝苯地平后,激肽释放酶和前列腺素E的尿排泄量也分别显著增加了29.4%和50.0%。尿激肽释放酶排泄量的变化与尿量变化(r = 0.70,p < 0.01)或尿钠排泄量变化(r = 0.86,p < 0.01)显著相关。此外,尿前列腺素E排泄量的变化也与尿量变化(r = 0.72,p < 0.01)或尿钠排泄量变化(r = 0.53,p < 0.05)显著相关。尽管血浆肾素活性显著增加,但血浆醛固酮浓度并未改变,且服用硝苯地平后血浆醛固酮浓度/血浆肾素活性比值降低。这些结果表明,增强的肾激肽释放酶 - 激肽 - 前列腺素系统和醛固酮分泌受抑制可能与硝苯地平的利尿和利钠作用有关,并可能有助于降低主要由其血管舒张作用引起的血压。

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