By using receptor blockade, HPLC, destroying catecholaminergic nerve terminals by 6-OHDA, autoradiography, and other techniques, the relationship between effects of the spinal PCP receptor on cardiovascular function and noradrenergic system was studied. The main results were as following. Hypotension and bradycardia induced by ith PCP were significantly antagonized by prazosin and yohimbine; the MHPG levels in spinal CSF were significantly increased during the ith PCP induced hypotension and bradycardia; pretreatment with 6-OHDA to destroy NA terminals in the spinal cord significantly decreased the ith PCP induced hypotension and bradycardia, and the density of PCP receptors in the spinal cord. The results suggest that there are PCP receptors on the NA terminals in the spinal cord, which promoted the release of NA and/or inhibited the reuptake of NA. This may be a possible mechanism underlying the influence of spinal PCP receptors on cardiovascular function.