ABSTRACT
The present study was aimed to determine the role of K channels in the urocortin-induced endothelium-dependent and -independent relaxation in the rat left anterior descending coronary artery. Urocortin induced both endothelium-dependent and -independent relaxations. Removal of the endothelium reduced the relaxant effect of urocortin. In endotheliumintact rings pretreated with NG-nitro-L-arginine methyl ester or ODQ, the urocortin-induced relaxation was similar to that observed without endothelium. Ba2 inhibited the response to urocortin. Combined treatment with NG-nitro-L-arginine methyl ester did not cause further inhibition. In urocortin-relaxed rings, Ba2 or tetraethylammonium ions induced concentrationdependent contractions. Urocortin produced greater relaxations in rings without endothelium contracted by U46619 than by elevated extracellular K. Both tetraethylammonium ions and iberiotoxin inhibited the urocortin-induced endothelium-independent relaxation. In contrast, apamin, Ba2, and glibenclamide were ineffective. The present results indicate that endothelial nitric oxide and subsequent activation of Ba2-sensitive K channels is likely to be responsible for urocortin-induced endothelium-dependent relaxations, while activation of Ca2-activated K channels may partly mediate the endothelium-independent relaxations to urocortin.
