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单次口服卡托普利后尿激肽释放酶排泄与血压反应之间的关系。

Relation between urinary kallikrein excretion and blood pressure response to a single oral dose of captopril.

作者信息

Madeddu P, Oppes M, Rubattu S, Bandiera F, Dessi-Fulgheri P, Glorioso N, Soro A, Troffa M C, Rappelli A

出版信息

Clin Exp Hypertens A. 1987;9(2-3):615-21. doi: 10.3109/10641968709164233.

Abstract

Thirty-one essential hypertensives with normal or low PRA were evaluated before and after a single oral dose (50 mg) of captopril. A significant fall both in systolic and diastolic blood pressure (BP) was obtained in the subgroup of patients who were classified as "normal kallikrein hypertensives", while no significant change in BP was observed in "low kallikrein hypertensives". Furthermore the mean percentage fall in mean BP, throughout the 2 hours following captopril administration, was significantly related to the basal value of urinary kallikrein excretion (r = 0.47 p less than 0.05) in the entire group of patients. Our results suggest that a blunted activity of the kallikrein system might be responsible for failure of captopril in lowering BP in patients in whom the renin-angiotensin system is not pathogenetically implicated.

摘要

对31例血浆肾素活性(PRA)正常或降低的原发性高血压患者,在单次口服卡托普利(50mg)前后进行了评估。在被归类为“正常激肽释放酶高血压患者”的亚组中,收缩压和舒张压(BP)均显著下降,而“低激肽释放酶高血压患者”的血压未观察到显著变化。此外,在整个卡托普利给药后的2小时内,平均血压下降的平均百分比与整个患者组中尿激肽释放酶排泄的基础值显著相关(r = 0.47,p<0.05)。我们的结果表明,在肾素-血管紧张素系统未涉及发病机制的患者中,激肽释放酶系统活性减弱可能是卡托普利降低血压失败的原因。

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