Olmos G, Miralles A, Barturen F, García-Sevilla J A
Department of Fundamental Biology and Health Sciences, University of the Balearic Islands, Palma de Mallorca, Spain.
Eur J Pharmacol. 1991 Nov 19;205(1):93-6. doi: 10.1016/0014-2999(91)90776-m.
The specific binding of the agonist [corrected], [3H]clonidine, to neural membranes and clonidine-induced mydriasis were used to evaluate the density and sensitivity [corrected] of alpha 2-adrenoceptors in the brain of spontaneously hypertensive rats (SHR) and sex- and age-matched normotensive Wistar-Kyoto (WKY) rats. In hypertensive rats (SHR) the density of alpha 2-adrenoceptors was reduced in the cerebral cortex, hypothalamus and medulla oblongata (20-27%), as was the dose-pupillary response curve for clonidine (1.8-fold). The results demonstrated that this model of genetic hypertension is associated with desensitization of alpha 2-adrenoceptors in the brain.
使用激动剂[校正后]、[3H]可乐定与神经膜的特异性结合以及可乐定诱导的瞳孔散大,来评估自发性高血压大鼠(SHR)以及性别和年龄匹配的正常血压Wistar-Kyoto(WKY)大鼠脑中α2-肾上腺素能受体的密度和敏感性[校正后]。在高血压大鼠(SHR)中,大脑皮质、下丘脑和延髓中α2-肾上腺素能受体的密度降低(20%-27%),可乐定的剂量-瞳孔反应曲线也降低(1.8倍)。结果表明,这种遗传性高血压模型与脑中α2-肾上腺素能受体的脱敏有关。