可乐定中枢降压作用与中枢胆碱能神经系统的关系

从猫第四脑室给药。毒扁豆碱降压作用可被阿托品及育亨宾阻断;可乐定降压作用可被育亨宾、密胆碱及阿托品阻断,不被可卡因阻断,破坏中枢去甲肾上腺素能末梢后,阿托品的阻断作用消失;可乐定减少脑室灌流液Ach释出量。提示猫延髓胆碱能和去甲肾上腺素能神经在心血管调节功能上相互影响,它们似有可能同在一心血管神经原形成突触联系共同对血压行抑制性调节;可乐定可能通过激动通路上突触后α₂受体产生降压作用。

RELATIONSHIP BETWEEN THE HYPOTENSIVE EFFECT OF CLONIDINE AND THE CENTRAL CHOLINERGIC NERVOUS SYSTEM

Experiments were performed on 105 anesthetized cats. The drugs were injected into the fourth ventricule. The hypotensive effects of both physostigmine and clonidine were blocked by atropine and yohimbine. The results of peripheral experiments suggest that atropine blocks the hypotensive effect of clonidine not through central α-receptor blockade mechanism. After the central noradrenergic nerve terminal was destroyed by 6-OHDA, the hypotensive effect of clonidine was no longer blocked by atropine. This suggests that an intact noradrenergic nerve in lower brain stem is essential for the blocking effect of atropine. Clonidine could decrease the Ach transmitter release in the overflow of brain ventricular infusion, and the hypotensive effect of clonidine could be blocked by hemicholine.Cocaine did not affect the hypotensive effect of clonidine. Methoxamine did not induce hypotensive effect. It appears that clonidine produces hypotensive effect through activating the central post-synaptic α₂-receptor.It appears that the cholinergic and the noradrenergic nerves synapse on the same cardiovascular neurone in the cat medulla oblongata. When the trigger receptors, Mreceptor and α₂-receptor, are activated, both receptors may induce the same inhibitory effect on blood pressure regulation, and clonidine produces hypotensive effect by activating post-synaptic α₂-receptor on this pathway. There seems to be no direct connexion between the hypotensive effect of clonidine and the central cholinergic nerve.