Chloroethylclonidine is a partial α1-adrenoceptor agonist in aorta and caudal arteries of the Wistar Kyoto rat

Abstract

The interaction between chloroethylclonidine ( N- β-chloroethyl- N-methylamino-methyl-clonidine) and α 1-adrenoceptors mediating contraction in Wistar Kyoto rat arteries was examined. In caudal ( α 1A-adrenoceptors) and aorta ( α 1D-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 α 1A-adrenoceptors as an irreversible partial agonist, inducing vascular contraction probably due to Ca 2+ mobilisation, and with aorta α 1D-adrenoceptors as a partial agonist, inducing slow-onset muscular contraction.