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激肽释放酶-激肽系统与高血压之间的相互关系:综述

Interrelationship between the kallikrein-kinin system and hypertension: a review.

作者信息

Sharma J N

机构信息

Department of Pharmacology, School of Medical Sciences, Universiti Sains Malaysia, Penang.

出版信息

Gen Pharmacol. 1988;19(2):177-87. doi: 10.1016/0306-3623(88)90058-4.

Abstract

The evidence presented here suggests strongly that the kallikreins-kininogens-kinins-kininase II system has most significant role in regulation of systemic BP. This system is involved in mediation and modulation of renin-angiotensin-aldosterone, PGS and vasopressin in the regulation of sodium water balance, renal hemodynamic and BP. Therefore, reduction in the kinin-formation due to high production of kininase II, and lower formation of tissue kallikrein might result in an increased release of vasoconstrictor angiotensin II on one side, and on the other side much reduced production of PGE, vasodilator. These changes might lead to deranged vascular smooth muscle structures and cell membrane functions, retention of sodium and water, increased plasma volume, and renovascular constriction. These physiological defects might result in the development of essential hypertension (Fig. 4). Although, it is possible now to treat hypertensive conditions with tissue kallikrein and kininase II inhibitors. These discoveries have opened up new vistas to research on the pharmacological applications of kallikreins-kininogens-kinins-kininases in human diseases.

摘要

此处所呈现的证据有力地表明,激肽释放酶-激肽原-激肽-激肽酶II系统在系统性血压调节中发挥着最为重要的作用。该系统在肾素-血管紧张素-醛固酮、前列腺素和血管加压素调节钠水平衡、肾血流动力学及血压的过程中参与介导与调节。因此,一方面,激肽酶II的高产量导致激肽生成减少,组织激肽释放酶生成降低;另一方面,血管舒张剂前列腺素E生成大幅减少。这些变化可能导致血管平滑肌结构和细胞膜功能紊乱、钠水潴留、血容量增加以及肾血管收缩。这些生理缺陷可能导致原发性高血压的发生(图4)。尽管目前可以用组织激肽释放酶和激肽酶II抑制剂来治疗高血压病症。这些发现为激肽释放酶-激肽原-激肽-激肽酶在人类疾病中的药理学应用研究开辟了新视野。

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