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肾去神经支配后大鼠单肾单夹高血压的发病机制

Pathogenesis of one-kidney, one-clip hypertension in rats after renal denervation.

作者信息

Villarreal D, Freeman R H, Davis J O, Garoutte G, Sweet W D

出版信息

Am J Physiol. 1984 Jul;247(1 Pt 2):H61-6. doi: 10.1152/ajpheart.1984.247.1.H61.

DOI:10.1152/ajpheart.1984.247.1.H61
PMID:6377927
Abstract

This study examines the role of the renal nerves in the chronic and early developmental stages of one-kidney, one-clip (1K-1C) Goldblatt hypertension. Groups of uninephrectomized Sprague-Dawley rats underwent renal artery constriction with a clip of an internal diameter of 0.23 mm (groups 1 and 3) or 0.40 mm (groups 2 and 4) to produce severe or moderate hypertension. Two weeks later, groups 1 and 2 were subjected to renal denervation and groups 3 and 4 were denervated 6 and 7 wk after clipping, respectively. In all four groups, hypertension remained unchanged during the subsequent 2 wk after denervation. To study further the effects of renal denervation during the early onset of hypertension, groups 5, 6, and 7 received the smaller (0.23 mm) clip after uninephrectomy. Groups 5 and 6 were renal denervated immediately before clipping; group 7 was not denervated. In groups 6 and 7 the renin-angiotensin system was blocked with a continuous infusion of the converting-enzyme inhibitor captopril for 24 h before and 15 days after clipping. In group 5, renal denervation did not prevent a prompt and severe rise in the systolic blood pressure. In groups 6 and 7, infusion of captopril prevented the hypertension only during the first 4 days after clipping; at no time was there a difference in the systolic blood pressure curves of groups 6 and 7 during or after captopril infusion. These data demonstrate that regardless of the severity and duration of hypertension, renal denervation failed to attenuate either the development or the maintenance of 1K-1C Goldblatt hypertension in the rat. Thus the present results fail to provide support for the concept that the renal nerves modulate the hypertension in this experimental model.

摘要

本研究探讨肾神经在单肾单夹(1K-1C)戈德布拉特高血压慢性及早期发育阶段中的作用。将未切除一侧肾脏的斯普拉格-道利大鼠分组,用内径为0.23毫米的夹子(第1组和第3组)或0.40毫米的夹子(第2组和第4组)对肾动脉进行缩窄,以产生重度或中度高血压。两周后,第1组和第2组接受肾去神经支配,第3组和第4组分别在夹闭后6周和7周去神经支配。在所有四组中,去神经支配后的随后2周内高血压均无变化。为进一步研究高血压早期发作时肾去神经支配的影响,第5、6和7组在切除一侧肾脏后接受较小(0.23毫米)的夹子。第5组和第6组在夹闭前立即进行肾去神经支配;第7组未去神经支配。在第6组和第7组中,在夹闭前24小时和夹闭后15天持续输注转化酶抑制剂卡托普利以阻断肾素-血管紧张素系统。在第5组中,肾去神经支配未能阻止收缩压迅速且严重升高。在第6组和第7组中,输注卡托普利仅在夹闭后的前4天预防了高血压;在输注卡托普利期间或之后,第6组和第7组的收缩压曲线在任何时候均无差异。这些数据表明,无论高血压的严重程度和持续时间如何,肾去神经支配均未能减弱大鼠1K-1C戈德布拉特高血压的发展或维持。因此,目前的结果未能支持肾神经调节该实验模型中高血压的概念。

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引用本文的文献

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