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肾血管性高血压中肾小球血管紧张素II受体密度的调节:对交感神经和血管加压素影响减弱的反应

Regulation of glomerular angiotensin II receptor densities in renovascular hypertension: response to reduced sympathetic and vasopressin influence.

作者信息

Sahlgren B, Eklöf A C, Aperia A

机构信息

Department of Pediatrics, St Göran's Children's Hospital, Karolinska Institute, Stockholm, Sweden.

出版信息

Acta Physiol Scand. 1992 Dec;146(4):467-71. doi: 10.1111/j.1748-1716.1992.tb09448.x.

Abstract

The regulation of the density of angiotensin II receptors in renal glomeruli in response to changes in salt intake is altered in Sprague-Dawley rats with renovascular hypertension due to aortic constriction, and in hypertensive salt-sensitive Dahl rats (Sahlgren 1989, Sahlgren & Aperia 1989). This study examines the modulatory role of sympathetic activity and arginine-vasopressin on angiotensin II receptors in hypertensive Sprague-Dawley rats with aortic constriction as well as in normotensive control rats. Denervation of the left kidney caused a 50% increase in the glomerular angiotensin II receptor density in the denervated kidney in both hypertensive rats and normotensive controls. An even more marked increase in glomerular receptor density occurred in both hypertensive rats and controls after blocking the sympathetic nervous system with guanethidine. To block the effects of arginine-vasopressin we used a blocker of the V1-receptors (predominant in vessels) and found an approximately 100% increase in the glomerular receptor density of angiotensin II in rats with aortic constriction. There was no reduction in blood pressure. Thus, on the receptor level the renin-angiotensin system is markedly influenced by the activity of other major pressor systems.

摘要

由于主动脉缩窄导致肾血管性高血压的Sprague-Dawley大鼠以及高血压盐敏感型Dahl大鼠中,肾小球血管紧张素II受体密度对盐摄入量变化的调节作用发生改变(Sahlgren,1989年;Sahlgren和Aperia,1989年)。本研究考察了交感神经活动和精氨酸加压素对主动脉缩窄的高血压Sprague-Dawley大鼠以及正常血压对照大鼠中血管紧张素II受体的调节作用。对左肾去神经支配后,高血压大鼠和正常血压对照大鼠去神经支配的肾脏中,肾小球血管紧张素II受体密度增加了50%。用胍乙啶阻断交感神经系统后,高血压大鼠和对照大鼠的肾小球受体密度均出现更为显著的增加。为阻断精氨酸加压素的作用,我们使用了一种V1受体(主要存在于血管中)阻滞剂,发现主动脉缩窄大鼠中血管紧张素II的肾小球受体密度增加了约100%。血压并未降低。因此,在受体水平上,肾素-血管紧张素系统受到其他主要升压系统活动的显著影响。

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