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自发性高血压大鼠激肽释放酶排泄增加及其被6-羟基多巴胺抑制

Increased kallikrein excretion in spontaneously hypertensive rats and its inhibition by 6-hydroxydopamine.

作者信息

Rascher W, Bönner G, Stocker M, Gross F

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1980 Aug;313(2):155-7. doi: 10.1007/BF00498573.

Abstract

Urinary kallikrein excretion was studied in young, stroke-prone, spontaneously hypertensive rats (spSHR). Seven-week-old spSHR were found to excrete more kallikrein into the urine than normotensive Wistar Kyoto control rats (WKR). "Chemical sympathectomy", induced by 6-hydroxydopamine (6-OHDA) immediately after birth, resulted in normotensive blood-pressure levels and in a reduction of kallikrein in spSHR. In normotensive WKR, blood pressure and urinary kallikrein excretion were only slightly diminished by 6-OHDA. The results suggest a relationship between sympathetic activity and kallikrein excretion, being especially pronounced in spSHR, which have an elevated sympathetic activity.

摘要

对年轻的、易中风的自发性高血压大鼠(spSHR)的尿激肽释放酶排泄情况进行了研究。发现7周龄的spSHR比正常血压的Wistar Kyoto对照大鼠(WKR)向尿液中排泄更多的激肽释放酶。出生后立即用6-羟基多巴胺(6-OHDA)诱导的“化学交感神经切除术”导致spSHR血压正常化,并使激肽释放酶减少。在正常血压的WKR中,6-OHDA仅使血压和尿激肽释放酶排泄略有减少。结果表明交感神经活动与激肽释放酶排泄之间存在关联,在交感神经活动升高的spSHR中尤为明显。

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