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肾激肽释放酶系统、血容量及肾性高血压。

Renal kallikrein system, volemia, and renal hypertension.

作者信息

Rosas R, Albertini R, Croxatto H R

出版信息

Mayo Clin Proc. 1977 Jul;52(7):459-61.

PMID:875470
Abstract

Plasma, blood, and urine volumes, renal kallikrein, and arterial pressure were measured in control and renal hypertensive rats in order to study the role of the renal kallikrein system in regulating arterial pressure and its relation with the alterations in water handling observed in hypertension. A decrease in kallikrein content of the kidney (157 +/- 17 versus 236 +/- 16 ng bradykinin equivalents per gram of tissue in control rats) was associated with an increase in plasma volume (38.0 "/- 1.6 versus 32.0 +/- 0.9 ml/kg body weight in control rats) and an increase in urine volume (45.5 +/- 4.9 versus 20.3 +/- 1.6 ml/kg body weight per 24 hours in control rats). No linear correlation was found between these factors and the arterial pressure of hypertensive animals. These findings support the hypothesis that changes in renal kallikrein are more directly related to water and electrolyte metabolism than to the arterial pressure regulation. Our results also suggest an interaction between the kallikrein-kinin and the renin-angiotensin-aldosterone systems. The possible relations of both enzymatic systems to the regulation of arterial pressure and of water-electrolyte handling are summarized schematically.

摘要

为了研究肾激肽释放酶系统在调节动脉血压中的作用及其与高血压时水代谢改变的关系,对正常大鼠和肾性高血压大鼠的血浆、血液及尿量、肾激肽释放酶和动脉血压进行了测量。肾激肽释放酶含量降低(正常大鼠每克组织中缓激肽当量为236±16 ng,而肾性高血压大鼠为157±17 ng)与血浆量增加(正常大鼠为32.0±0.9 ml/kg体重,肾性高血压大鼠为38.0±1.6 ml/kg体重)及尿量增加(正常大鼠每24小时为20.3±1.6 ml/kg体重,肾性高血压大鼠为45.5±4.9 ml/kg体重)相关。在这些因素与高血压动物的动脉血压之间未发现线性关系。这些发现支持这样的假说,即肾激肽释放酶的变化与水和电解质代谢的关系比与动脉血压调节的关系更为直接。我们的结果还提示激肽释放酶 - 激肽系统与肾素 - 血管紧张素 - 醛固酮系统之间存在相互作用。对这两个酶系统与动脉血压调节及水 - 电解质处理的可能关系进行了示意性总结。

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