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大鼠肾脏中体液介导的降压系统:一种生理性降压机制?

The humorally mediated antihypertensive system of the rat kidney: a physiological depressor mechanism?

作者信息

Karlström G, Göthberg G

机构信息

Department of Physiology, University of Gothenburg, Sweden.

出版信息

J Hypertens Suppl. 1987 Dec;5(5):S91-4.

PMID:3481822
Abstract

The humoral renomedullary antihypertensive system, described by Muirhead [1], is known to be strongly activated upon unclipping renal hypertensive rats. The present study was designed to determine whether this system is tonically active in normotensive rat kidneys at normotensive pressure levels. Anaesthetized normotensive donor rats (NDR) were used to perfuse an isolated age-matched normotensive recipient (NRR) kidney, via an extracorporal circuit, set at different perfusion pressures, while the NDR mean arterial pressure and heart rate were measured continuously. The results showed non-significant alterations in the NDR heart rate and mean arterial pressure at 80 mmHg NRR kidney perfusion pressure, while at 100 and 150 mmHg there were significant, dose-dependent and gradual reductions in both the heart rate and mean arterial pressure in NDR. We conclude that the renal humoral antihypertensive system is active in normotensive kidneys already in the normotensive pressure range, but becomes further engaged in a dose-dependent way when renal perfusion pressure is raised.

摘要

由缪尔黑德[1]所描述的体液性肾髓质抗高血压系统,已知在解除肾性高血压大鼠的夹闭后会被强烈激活。本研究旨在确定该系统在正常血压水平的正常血压大鼠肾脏中是否持续发挥作用。使用麻醉的正常血压供体大鼠(NDR),通过体外循环,以不同的灌注压力对一只年龄匹配的正常血压受体(NRR)离体肾脏进行灌注,同时持续测量NDR的平均动脉压和心率。结果显示,在NRR肾脏灌注压力为80 mmHg时,NDR的心率和平均动脉压无显著变化,而在100 mmHg和150 mmHg时,NDR的心率和平均动脉压均出现显著的、剂量依赖性的逐渐降低。我们得出结论,肾体液性抗高血压系统在正常血压范围内的正常血压肾脏中已然发挥作用,但当肾灌注压力升高时,它会以剂量依赖性方式进一步发挥作用。

相似文献

1
The humorally mediated antihypertensive system of the rat kidney: a physiological depressor mechanism?大鼠肾脏中体液介导的降压系统:一种生理性降压机制?
J Hypertens Suppl. 1987 Dec;5(5):S91-4.
2
Is the humoral renal antihypertensive activity of the spontaneously hypertensive rat (SHR) reset to the high blood pressure?自发性高血压大鼠(SHR)的体液性肾性降压活性是否会因高血压而调整?
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Acta Physiol Scand. 1995 Oct;155(2):183-91. doi: 10.1111/j.1748-1716.1995.tb09963.x.
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J Physiol. 2002 Feb 1;538(Pt 3):901-10. doi: 10.1113/jphysiol.2001.013280.