尿钾激肽在正常妊娠和高血压妊娠中的作用。

O A Elebute, I H Mills
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引用次数: 0

摘要

在正常妊娠妇女和妊娠晚期高血压妇女中测量尿钾激肽。平均尿钾激肽在妊娠早期最高,在妊娠晚期显著下降到非孕酮系统。正常妊娠时尿钾激肽与妊娠期长度呈负相关。高血压患者尿钾激肽显著低于未怀孕时的水平,而在同一天,钠和水的肾脏排泄与正常妊娠没有什么不同,根据已知的增加钾激肽排泄的因素进行了讨论。这种升高不太可能是由于孕期高醛固酮对钠保留作用的逃逸。这可能部分是由于血管紧张素II水平升高的刺激作用,但它被认为最有可能是循环肾血管扩张剂的作用。妊娠期高血压的钾化肽减少可能与高血压的发展有关,类似于原发性高血压的钾化肽分泌减少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Urinary kallikrein in normal and hypertensive pregnancies.

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.

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