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正常妊娠和高血压妊娠中的尿激肽释放酶

Urinary kallikrein in normal and hypertensive pregnancies.

作者信息

Elebute O A, Mills I H

出版信息

Perspect Nephrol Hypertens. 1976;5:329-38.

PMID:1005045
Abstract

Urinary kallikrein was measured in normal pregnant women stages of gestation and in women who developed hypertension in late pregnancy. Mean urinary kallikrein was highest in the first trimester and fell significantly in the third trimester to nonpregnosterone system. A negative correlation was observed between urinary kallikrein and the length of gestation in normal pregnancy. Urinary kallikrein fell significantly below nonpregnant levels in patients with hypertension while the renal excretion of sodium and water was not different from that in normal pregnancy of the same dy is discussed in the light of factors known to increase kallikrein excretion. It is considered unlikely that this elevation is due to the escape from the sodium-retaining effect of the high aldosterone of pregnancy. It may be due in part to the stimulating effect of raised angiotensin II levels but it is considered most likely to be the effect of a circulating renal vasodilator. The reduced kallikrein in hypertension of pregnancy may play a part in the development of the hypertension and resembles the reduced kallikrein excretion in essential hypertension.

摘要

对正常孕妇不同妊娠阶段以及妊娠晚期出现高血压的女性进行了尿激肽释放酶的测定。尿激肽释放酶均值在孕早期最高,在孕晚期显著下降至非孕期水平。在正常妊娠中,尿激肽释放酶与妊娠时长呈负相关。高血压患者的尿激肽释放酶显著低于非孕期水平,而钠和水的肾排泄与相同孕周的正常妊娠并无差异。本文根据已知会增加激肽释放酶排泄的因素,对这一现象进行了讨论。认为这种升高不太可能是由于对孕期高醛固酮钠潴留作用的逃逸。部分可能是由于血管紧张素 II 水平升高的刺激作用,但最有可能是循环肾血管扩张剂的作用。妊娠高血压中激肽释放酶减少可能在高血压的发生中起作用,这与原发性高血压中激肽释放酶排泄减少相似。

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