Abstract: 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.