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肾去神经支配可使清醒大鼠高肾素性高血压的血压及压力感受器反射恢复正常。

Renal denervation normalizes pressure and baroreceptor reflex in high renin hypertension in conscious rats.

作者信息

Oliveira V L, Irigoyen M C, Moreira E D, Strunz C, Krieger E M

机构信息

Heart Institute, University Hospital, Faculty of Medicine, University of São Paulo, Brazil.

出版信息

Hypertension. 1992 Feb;19(2 Suppl):II17-21. doi: 10.1161/01.hyp.19.2_suppl.ii17.

Abstract

High renin hypertension is usually accompanied by impairment of the baroreceptor reflexes. This feature has been mostly ascribed to overactivity of the renin-angiotensin system. However, renal nerves could also modulate the baroreceptor reflexes. In the present experiments, the effect of renal denervation on the depressed baroreceptor reflexes was studied in rats subjected to aortic ligation between the renal arteries. Renal denervation of the ischemic kidney was performed at the same time as aortic ligation. The resulting effects on arterial pressure, heart rate, plasma renin activity, and baroreceptor reflex control of heart rate were studied 10-12 days after ligation and denervation. Aortic ligation induced high levels of mean arterial pressure (166 +/- 6 versus 110 +/- 3 mm Hg in controls), heart rate (380 +/- 9 versus 352 +/- 8 beats per minute in controls), and plasma renin activity (44 +/- 5 versus 6 +/- 1.2 ng angiotensin I/ml/hr). The baroreceptor reflex sensitivity for bradycardia and tachycardia was significantly reduced (-0.18 +/- 0.04 and -0.18 +/- 0.05, respectively, versus -2.3 +/- 0.01 and -2.4 +2- 0.1 beats per minute per mm Hg in controls). Denervation of the ischemic kidney attenuated the development of hypertension in aortic-ligated rats (122 +/- 3 mm Hg), lowering heart rate (319 +/- 8 beats per minute) and normalizing baroreceptor reflex sensitivity to bradycardia (-2.0 +/- 0.2 beats per minute per mm Hg) and to tachycardia (-4.0 +/- 0.1 beats per minute per mm Hg). Plasma renin activity was also normalized (4.3 +/- 2.4 ng angiotensin I/ml/hr).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

高肾素性高血压通常伴有压力感受器反射受损。这一特征大多归因于肾素 - 血管紧张素系统的过度活跃。然而,肾神经也可调节压力感受器反射。在本实验中,在肾动脉之间进行主动脉结扎的大鼠中研究了肾去神经支配对减弱的压力感受器反射的影响。在进行主动脉结扎的同时对缺血肾进行肾去神经支配。在结扎和去神经支配后10 - 12天研究其对动脉血压、心率、血浆肾素活性以及心率的压力感受器反射控制的影响。主动脉结扎导致平均动脉压(166±6 mmHg,而对照组为110±3 mmHg)、心率(380±9次/分钟,而对照组为352±8次/分钟)和血浆肾素活性(44±5 ng血管紧张素I/ml/小时,而对照组为6±1.2 ng)升高。压力感受器对心动过缓和心动过速的反射敏感性显著降低(分别为 - 0.18±0.04和 - 0.18±0.05,而对照组为 - 2.3±0.01和 - 2.4±0.1次/分钟/mmHg)。缺血肾去神经支配减弱了主动脉结扎大鼠的高血压发展(122±3 mmHg),降低了心率(319±8次/分钟),并使压力感受器对心动过缓和心动过速的反射敏感性恢复正常(分别为 - 2.0±0.2次/分钟/mmHg和 - 4.0±0.1次/分钟/mmHg)。血浆肾素活性也恢复正常(4.3±2.4 ng血管紧张素I/ml/小时)。(摘要截断于250字)

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