脊髓苯环立啶受体的心血管效应与去甲肾上腺素能系统

RELATIONSHIP BETWEEN SPINAL PCP RECEPTOR ON CARDIOVASCULAR EFFECT AND NORADRENERGIC SYSTEM

本文应用受体阻断、高效液相,6-OHDA 化学损毁神经末梢和放射自显影等多学科技术方法,探讨脊髓苯环立啶受体的心血管效应与去甲肾上腺素能神经系统的关系。结果表明,哌唑嗪、育亨宾均可对抗 ith PCP 的降压和减慢心率作用,ith PCP 产生降压和减慢心率作用时,脊髓脑脊液内 MHPG 的含量升高;用6-OHDA 损毁脊髓 NA 能神经末梢后,ith PCP的降压和减慢心率作用大为减弱,脊髓 PCP 受体密度亦同时大为降低。可以认为,脊髓内有 PCP 受体分布于 NA 能神经末梢上,促进 NA 释放或抑制 NA 重摄取,可能是脊髓 PCP 受体产生心血管抑制效应的重要机理。

By using receptor blockade,HPLC,destroying catecholaminergic nerveterminals by 6-OHDA,autoradiography,and other techniques,the relationshipbetween effects of the spinal PCP receptor on cardiovascular function and norad-renergic system was studied.The main results were as following.Hypoten-sion and bradycardia induced by ith PCP were significantly antagonized by pra-zosin and yohimbine;the MHPG levels in spinal CSF were significantly increasedduring the ith PCP induced hypotension and bradycardia;pretreatment with6-OHDA to destroy NA terminals in the spinal cord significantly decreased theith PCP induced hypotension and bradycardia,and the density of PCP receptorsin the spinal cord.The results suggest that there are PCP receptors on the NA terminals in thespinal cord,which promoted the release of NA and/or inhibited the reuptake ofNA.This may be a possible mechanism underlying the influence of spinal PCPreceptors on cardiovascular function.