L-arginine-induced dilatation of goat coronary artery involves activation of K(ATP) channels

In the present study, the mechanism of relaxant response of nitric oxide precursor, L-arginine, was investigated in goat isolated coronary artery. L-arginine (1 mM) reversed the U-46619 (1 microM)-induced contraction both in endothelium-intact and endothelium-denuded arterial ring preparations. L-arginine analogues, L-NAME, L-NNA and L-NMMA and the guanylyl cyclase inhibitor, methylene blue failed to attenuate the relaxant response of L-arginine. These observations negate the involvement of nitric oxide in mediating the relaxation by L-arginine. K(ATP) channel blocker, glibenclamide (3 microM), abolished the vasorelaxant responses of L-arginine in endothelium-denuded preparations, thereby suggesting the involvement of KATP channels. Further, L-arginine also failed to induce relaxation of the coronary arterial rings constricted with K+ (80 mM)-PSS. Taken together, the results of the present study suggest that L- arginine relaxes goat isolated coronary artery through activation of K(ATP) channels.