The influence of chloroethylclonidine-induced contraction in isolated arteries of Wistar Kyoto rats: alpha(1D)- and alpha(1A)-adrenoceptors, protein kinase C, and calcium influx

Background. It has recently been reported that chloroethylclonidine (CEC) e licited contraction in tail arteries (alpha (1A)-adrenoceptors) and aorta ( alpha (1D)-adrenoceptors) from normotensive and spontaneously hypertensive rats (SHR). This study investigated the relationship between CEC-induced co ntraction and the role of protein kinase C (PKC) and extracellular Cati inf lux in tail arteries and aorta from Wistar Kyoto rats (WKY). Methods. Time-course of CEC-induced contraction in endothelium-denuded arte ries from Wistar, WKY, and SHR rats was evaluated. In WKY arteries, calphos tin C (1 x 10(-6) M) and nitrendipine (1 x 10(-6) M) were used to determine the role of PKC and extracellular Ca++ in the contractile response to CECI respectively. Results. Chloroethylclonidine (1 x 10(-4) M) elicited contraction in tail a rteries and aorta from normotensive and hypertensive rats. Maximal response to CEC was similar in tail arteries among strains (approximate to 30% of n orepinephrine effect), while in aorta CEC elicited a higher contraction in WKY and SHR than in Wistar (59, 86, and 18% of norepinephrine effect, respe ctively). CEC-elicited maximal contractile responses were reached in 5 min in tail arteries and in 30-45 min in aorta irrespective of the rat strain, suggesting that different intracellular signaling pathways are involved in the contractile response to CEC in these arteries. In WKY tail arteries, ca lphostin C and nitrendipine blocked CEC-induced contraction while in aorta nitrendipine, but not calphostin C, inhibited CEC action. Conclusions. This study confirms marked strain-dependent differences in rat aorta responsiveness to CEC and suggests a central role for PKC in respons e to CEC in tail arteries and for extracellular Ca++ influx in aorta. (C) 2 001 IMSS. Published by Elsevier Science Inc.