Chloroethylclonidine is a partial alpha1-adrenoceptor agonist in aorta and caudal arteries of the Wistar Kyoto rat.

The interaction between chloroethylclonidine (N-beta-chloroethyl-N-methylamino-methyl-clonidine) and alpha1-adrenoceptors mediating contraction in Wistar Kyoto rat arteries was examined. In caudal (alpha1A-adrenoceptors) and aorta (alpha1D-adrenoceptors) arteries, chloroethylclonidine (10(-4) M) elicited contraction with different time frames (maximal effect within 4 min in the caudal artery and at 30-45 min in aorta). Phentolamine (10(-6) M) completely prevented chloroethylclonidine-induced contraction in aorta, but partially did so in the caudal artery. Rauwolscine (10(-7) M) partially prevented the chloroethylclonidine contractile effect in both arteries. Chloroethylclonidine attenuated the contractile effect of low concentrations of norepinephrine, however, maximal contraction was observed at catecholamine concentrations above 10(-7) M in the caudal artery and 10(-6) M in the aorta. It is concluded that chloroethylclonidine interacts with caudal alpha1A-adrenoceptors as an irreversible partial agonist, inducing vascular contraction probably due to Ca2+ mobilisation, and with aorta alpha1D-adrenoceptors as a partial agonist, inducing slow-onset muscular contraction.