Lo M, Julien C, Barres C, Medeiros I, Allevard A M, Vincent M, Sassard J
Département de Physiologie et Pharmacologie Clinique, Centre National de la Recherche Scientifique, Unité de Recherche Associée 606, Faculté de Pharmacie, Lyon, France.
Am J Physiol. 1991 Oct;261(4 Pt 2):R1052-6. doi: 10.1152/ajpregu.1991.261.4.R1052.
This study examined the contribution of the main pressor systems to the residual hypertension exhibited by genetically hypertensive (LH) rats of the Lyon strain after early chronic sympathectomy with guanethidine. Blood pressure (BP) was recorded in conscious LH and normotensive control (LN) rats, either intact or sympathectomized, during sequential blockade of the renin-angiotensin system, vasopressin receptors, the autonomic nervous system, and finally after maximal vasodilation with hydralazine. In sympathectomized rats 1) renin-angiotensin system blockade equally reduced BP in both strains, whether it was realized before (-20%) or after (-30%) vasopressin antagonism; 2) isolated vasopressin antagonism decreased BP in LH (-8%) but not in LN rats; 3) autonomic blockade and hydralazine induced additional decreases in BP that were similar in both strains; and 4) intermediate and final levels of BP remained always higher in LH than in LN rats. It is concluded that, after sympathectomy, BP is maintained primarily by the renin-angiotensin system. In sympathectomized LH rats, the maintenance of hypertension does not depend on hyperactivity of the main pressor systems but rather on an increase in the intrinsic vascular resistance that develops in the absence of the sympathetic innervation of the vessels.
本研究探讨了主要升压系统对利昂品系遗传性高血压(LH)大鼠在早期用胍乙啶进行慢性交感神经切除术后所表现出的残余高血压的作用。在依次阻断肾素 - 血管紧张素系统、血管升压素受体、自主神经系统,以及最后用肼屈嗪进行最大程度血管舒张后,对清醒的LH大鼠和正常血压对照(LN)大鼠(完整或交感神经切除)记录血压。在交感神经切除的大鼠中:1)肾素 - 血管紧张素系统阻断在两种品系中均能同等程度降低血压,无论其是在血管升压素拮抗之前(降低20%)还是之后(降低30%)实现;2)单独的血管升压素拮抗使LH大鼠血压降低(8%),但对LN大鼠无此作用;3)自主神经阻断和肼屈嗪诱导的血压进一步降低在两种品系中相似;4)LH大鼠的血压中间水平和最终水平始终高于LN大鼠。得出的结论是,交感神经切除术后,血压主要由肾素 - 血管紧张素系统维持。在交感神经切除的LH大鼠中,高血压的维持不依赖于主要升压系统的过度活跃,而是依赖于在血管缺乏交感神经支配的情况下所产生的内在血管阻力增加。