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组织激肽释放酶、血压调节与高血压:遗传激肽释放酶缺乏的启示。

Tissue kallikrein, blood pressure regulation, and hypertension: insight from genetic kallikrein deficiency.

机构信息

INSERM U872, Centre de Recherche des Cordeliers, 15 rue de l'Ecole de Medecine, F-75006 Paris, France.

出版信息

Biol Chem. 2013 Mar;394(3):329-33. doi: 10.1515/hsz-2012-0332.

Abstract

Tissue kallikrein has been suggested to be involved in blood pressure regulation and in protection against hypertension. However, this hypothesis remains debated. Recently, murine genetic models of kallikrein deficiency have been engineered and partial genetic deficiency in kallikrein activity has been characterized in humans. Studies in kallikrein-deficient mice indicate that kallikrein indeed influences blood pressure in the setting of mineralocorticoid excess and salt retention but not in normotensive animals and in high renin hypertension. These observations suggest that kallikrein can have antihypertensive function in physiological situations where sodium retention can trigger blood pressure elevation.

摘要

组织激肽释放酶被认为参与血压调节和预防高血压。然而,这一假说仍存在争议。最近,设计了激肽释放酶缺乏的鼠基因模型,并且在人类中对激肽释放酶活性的部分遗传缺乏进行了特征描述。激肽释放酶缺陷小鼠的研究表明,激肽释放酶确实会影响盐潴留和醛固酮过多时的血压,但不会影响正常血压动物和高肾素性高血压动物的血压。这些观察结果表明,在钠潴留可引发血压升高的生理情况下,激肽释放酶可能具有降压功能。

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