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作 者:郭涓[1] 殷伟平[1] 黄伟秋[1] 徐斌[1] 钱忠明[2]
机构地区:[1]苏州医学院生理学教研室,苏州215007 [2]香港理工大学应用生物及化学科技学系
出 处:《生理学报》1997年第1期110-114,共5页Acta Physiologica Sinica
摘 要:在戊巴比妥钠麻醉的大鼠,观察杏仁中央核(CeA)内微量注射促肾上腺皮质激素释放激素(CRH)对血压的影响,并对其中枢机制进行初步探讨。结果如下:(1)CeA内微量注射CRH产生剂量依赖性血压升高,这种升压效应一般出现在注射后5min左右,可维持1h以上。(2)CeA内给予CRH受体措抗剂α-helicalCRH9-41,能取消CeA内注射CRH引起的升压效应。(3)侧脑室内给予纳洛酮,显著减弱CeA内注射CRH引起的升压效应。(4)NTS内给予α-helicalCRH9-41,显著减弱CeA中CRH引起的升压效应。上述结果提示,CeA内微量注射CRH引起的升压效应可能部分是通过阿片系统起作用的,杏仁-孤束核的CRH通路可能是CeA中CRH引起血压升高的下行通路之一。The effect of microinjection of corticotropin releasing hormone (CRH) into the central nucleus of amygdala (CeA) on blood pressure was examined in Wistar rats anaesthetized with pentobarbital sodium. The results were as follows: (1) Microinjection ofCRH 100, 500 ng into the CeA produced a dose-dependent increase in blood pressure.The response occurred 5 min after injection and lasted for at least 1 h. (2) The response could be blocked by injection of CRH receptor antugonist a-helical CRH9-41 intoCeA- (3) Lateral ventricle injection of naloxone could also attenuate the pressor response of CRH. (4) After injection of a-helical CRH9-41 into nucleus of solitary tract,the pressor response of CRH was diminished. The results suggest that the pressor effectinduced by microinjection of CRH into the CeA might be pertly mediated through opioidsystem via a descending pathway from CeA to NTS.
分 类 号:R338.26[医药卫生—人体生理学]
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