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可乐定降低中枢交感神经输出前后高血压患者和正常血压者循环单核细胞上β-肾上腺素能受体的表达。

Expression of beta-adrenoceptors on circulating mononuclear cells in hypertensives and normotensives before and after reduction of central sympathetic outflow by clonidine.

作者信息

Zoukos Y, Thomaides T, Chaudhuri K R, Pavitt D V, Cuzner M L, Mathias C J

机构信息

Department of Neurochemistry, National Hospital for Neurology and Neurosurgery, London, UK.

出版信息

Blood Press. 1994 May;3(3):172-7. doi: 10.3109/08037059409102248.

DOI:10.3109/08037059409102248
PMID:8069405
Abstract

We have studied beta-adrenoceptor number and affinity on peripheral blood mononuclear cells (PBMCs) in normotensives (NT) and hypertensives (HT), before and after intravenous administration of clonidine, an alpha 2-adrenoceptor agonist which lowers blood pressure predominantly by reducing central nervous system sympathetic outflow. After clonidine, there was a decrease in blood pressure and plasma noradrenaline (NA) and adrenaline (Ad) levels, with an increase in growth hormone (GH) levels, in both NT and HT. There was no difference in basal beta-adrenoceptor densities on PBMCs between NT and HT. After clonidine at 30 and 60 min, there was an increase in beta-adrenoceptor density associated with a low affinity in NT. In HT, no changes were observed. The increased beta-adrenoceptor densities on PBMCs in NT after clonidine, returned to baseline values after 2 h. Short term up-regulation of beta-adrenoceptors on PBMCs in NT after clonidine is accompanied by a fall in blood pressure (BP) and plasma levels of catecholamines. The changes may represent a compensatory mechanism reflecting a rapid externalization-activation of adrenoceptors residing on the internal surface of the membranes with a change of the coupling ability between the receptor and the catalytic component. In HT, although the haemodynamic and neurohormonal response to clonidine was similar to NT, short term upregulation of receptors did not occur. The lack of such response may mirror a form of regulatory dysfunction of beta-adrenoceptors in HT.

摘要

我们研究了正常血压者(NT)和高血压患者(HT)静脉注射可乐定(一种主要通过减少中枢神经系统交感神经输出而降低血压的α2肾上腺素能受体激动剂)前后外周血单核细胞(PBMCs)上β肾上腺素能受体的数量和亲和力。注射可乐定后,NT组和HT组的血压、血浆去甲肾上腺素(NA)和肾上腺素(Ad)水平均下降,生长激素(GH)水平升高。NT组和HT组PBMCs上的基础β肾上腺素能受体密度无差异。注射可乐定后30分钟和60分钟,NT组β肾上腺素能受体密度增加且亲和力降低。在HT组中,未观察到变化。NT组注射可乐定后PBMCs上增加的β肾上腺素能受体密度在2小时后恢复到基线值。可乐定后NT组PBMCs上β肾上腺素能受体的短期上调伴随着血压(BP)和血浆儿茶酚胺水平的下降。这些变化可能代表一种代偿机制,反映了位于膜内表面的肾上腺素能受体的快速外化激活以及受体与催化成分之间偶联能力的变化。在HT组中,尽管对可乐定的血流动力学和神经激素反应与NT组相似,但受体的短期上调并未发生。这种反应的缺乏可能反映了HT组中β肾上腺素能受体的一种调节功能障碍形式。

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