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长期抑制血管紧张素II期间醛固酮血浆浓度升高。

Rise in plasma concentration of aldosterone during long-term angiotensin II suppression.

作者信息

Staessen J, Lijnen P, Fagard R, Verschueren L J, Amery A

出版信息

J Endocrinol. 1981 Dec;91(3):457-65. doi: 10.1677/joe.0.0910457.

Abstract

The plasma concentration of aldosterone was followed in seven hypertensive patients before and during long-term angiotensin II suppression with the orally active angiotensin-I-converting-enzyme inhibitor, captopril. The plasma concentration of aldosterone decreased initially from 74 to 21 pg/ml (P less than 0.05) after 1 month of administration of captopril. Thereafter the plasma concentration of aldosterone began to rise and after 1 year reached a level of 165 pg/ml. During long-term captopril therapy the plasma renin activity remained increased and the plasma angiotensin II concentration suppressed. The mechanism responsible for the late rise of the plasma concentration of aldosterone during long-term angiotensin II suppression with captopril remains to be elucidated. A sizeable and lasting hypotensive effect was observed in all patients.

摘要

对7名高血压患者在口服活性血管紧张素I转换酶抑制剂卡托普利长期抑制血管紧张素II之前和期间,监测其血浆醛固酮浓度。服用卡托普利1个月后,血浆醛固酮浓度最初从74 pg/ml降至21 pg/ml(P<0.05)。此后,血浆醛固酮浓度开始上升,1年后达到165 pg/ml的水平。在长期卡托普利治疗期间,血浆肾素活性持续升高,血浆血管紧张素II浓度受到抑制。卡托普利长期抑制血管紧张素II期间血浆醛固酮浓度后期升高的机制尚待阐明。所有患者均观察到显著且持久的降压效果。

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