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自发性高血压大鼠的肾血管阻力和反应性

Renal vascular resistance and reactivity in the spontaneously hypertensive rat.

作者信息

Fink G D, Brody M J

出版信息

Am J Physiol. 1979 Aug;237(2):F128-32. doi: 10.1152/ajprenal.1979.237.2.F128.

Abstract

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30--100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.

摘要

与正常血压的对照Wistar-Kyoto大鼠(WKY)相比,自发性高血压大鼠(SHR)的肾血管阻力升高。本研究在戊巴比妥麻醉的12至16周龄SHR和WKY的原位自体灌注肾脏中,研究了这种升高的血管阻力的可能决定因素。在很宽的动脉压范围(30 - 100 mmHg)内,WKY的肾血流量始终高于SHR。急性肾去神经支配并未改变这种相对流量差异,两种品系的肾血管阻力均降低约20%。还评估了肾血管阻力对肾神经刺激和动脉内血管活性激素给药的变化。两种品系肾脏对肾神经刺激、酪胺、血管紧张素II和乙酰胆碱的血管反应相似,但SHR肾脏对去甲肾上腺素的反应性明显较低。得出的结论是,SHR中升高的肾血管阻力并非源于对肾血管系统的过度神经源性影响,也不是源于对去甲肾上腺素或血管紧张素II的血管高反应性。

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