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激肽和前列环素在血压调节中的作用。

Role of kinins and prostacyclin in blood pressure regulation.

作者信息

Bönner G

机构信息

Department of internal medicine II, University of Cologne, FRG.

出版信息

Arch Mal Coeur Vaiss. 1989 Nov;82 Spec No 4:15-9.

PMID:2514656
Abstract

The main vasodepressor hormone systems are the kallikrein-kinin systems and the vascular prostacyclin. Kallikreins release kinins which are the biological active compounds of the kallikrein-kinin systems. Kinins are one of the most potent vasodilators reducing systemic blood pressure by diminution of vascular resistance. The reduction in blood pressure is strongly dose related. Prostacyclin develops similar effects on blood pressure as kinins. There is a close relationship between kinins and prostacyclin since kinins stimulate prostacyclin synthesis very effectively. In arterial hypertension there is a lack in kallikrein-kinin and prostacyclin activity. This could also be shown under experimental conditions in spontaneously hypertensive and in Dahl salt-sensitive rats. In clinical studies these experimental results were confirmed in primary hypertension. The blood pressure response to exogenous vasodepressor hormones is increased in hypertensives suffering from reduced endogenous vasodilator activity. In the knowledge of reduced vasodilator activities in primary hypertension the stimulation of kinins by prostacyclin will be of major interest in the management of primary hypertension. In the last years some drugs have been investigated with regard to their kinin prostacyclin stimulating effect, but only angiotensin converting enzyme inhibitors, linolenic acid and cicletanin seemed to induce therapeutic prostacyclin stimulation. However, it remains unclear whether these drugs develop their blood pressure lowering effect by stimulation of the discussed vasodilators or by some other effect.

摘要

主要的血管舒张激素系统是激肽释放酶 - 激肽系统和血管前列环素。激肽释放酶释放激肽,激肽是激肽释放酶 - 激肽系统的生物活性化合物。激肽是最有效的血管舒张剂之一,通过降低血管阻力来降低体循环血压。血压降低与剂量密切相关。前列环素对血压的影响与激肽相似。激肽与前列环素之间存在密切关系,因为激肽能非常有效地刺激前列环素的合成。在动脉高血压中,激肽释放酶 - 激肽和前列环素活性缺乏。这在自发性高血压大鼠和 Dahl 盐敏感大鼠的实验条件下也得到了证实。在临床研究中,这些实验结果在原发性高血压中得到了证实。内源性血管舒张剂活性降低的高血压患者对外源性血管舒张激素的血压反应增强。鉴于原发性高血压中血管舒张剂活性降低,前列环素对激肽的刺激在原发性高血压的治疗中将具有重要意义。近年来,已经对一些药物的激肽前列环素刺激作用进行了研究,但只有血管紧张素转换酶抑制剂、亚麻酸和西克莱他宁似乎能诱导治疗性前列环素刺激。然而,这些药物是通过刺激上述血管舒张剂还是通过其他作用来发挥其降压作用仍不清楚。

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