The Influence of Chloroethylclonidine-Induced Contraction in Isolated Arteries of Wistar Kyoto Rats: α1D- and α1A-Adrenoceptors, Protein Kinase C, and Calcium Influx

Background recently been reported that chloroethylclonidine (CEC) elicited contraction in tail arteries (α1A-adrenoceptors) and aorta (α1D-adrenoceptors) from normotensive and spontaneously hypertensive rats (SHR). This study investigated the relationship between CEC-induced contraction and the role of protein kinase C (PKC) and extracellular Ca++ influx in tail arteries and aorta from Wistar Kyoto rats (WKY). s ourse of CEC-induced contraction in endothelium-denuded arteries from Wistar, WKY, and SHR rats was evaluated. In WKY arteries, calphostin C (1 × 10−6 M) and nitrendipine (1 × 10−6 M) were used to determine the role of PKC and extracellular Ca+1 in the contractile response to CEC, respectively. s ethylclonidine (1 × 10−4 M) elicited contraction in tail arteries and aorta from normotensive and hypertensive rats. Maximal response to CEC was similar in tail arteries among strains (≈30% of norepinephrine effect), while in aorta CEC elicited a higher contraction in WKY and SHR than in Wistar (59, 86, and 18% of norepinephrine effect, respectively). 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, calphostin C and nitrendipine blocked CEC-induced contraction while in aorta nitrendipine, but not calphostin C, inhibited CEC action. sions tudy confirms marked strain-dependent differences in rat aorta responsiveness to CEC and suggests a central role for PKC in response to CEC in tail arteries and for extracellular Ca+1 influx in aorta.