DIHYDROPYRIDINE CA2-INDUCED RELAXATION THROUGH CYCLIC-GMP FORMATION IN PORCINE CORONARY-ARTERY( CHANNEL AGONISTS AND ANTAGONISTS POTENTIATEULTRAVIOLET LIGHT)

We investigated the mechanism of dihydropyridine Ca2+ channel agonist potentiation of ultraviolet (UV) light-induced smooth muscle relaxatio n in porcine coronary artery rings. Rings contracted with the dihydrop yridine Ca2+ channel agonist, (+)-S-202-791, were more sensitive to re laxation in response to UV light than were rings contracted with KCl o r histamine. Relaxation of (+)-S-202-791-contracted rings was independ ent of the presence of endothelium and was associated with cyclic GMP formation. Methylene blue (MB) prevented UV light-induced relaxation a nd cyclic GMP formation. UV light-induced relaxation of histamine and KCl contracted rings and cyclic GMP formation were potentiated by (+)- S-202-791 or the Ca2+ channel antagonist, (-)-R-202-791. Exposure of()-S-202-791 to UV light decreased its contractile potency. The data su ggest that UV light-induced relaxation of vascular smooth muscle (VSM) is mediated through cyclic GMP formation and that potentiation of UV light-induced relaxation by dihydropyridine Ca2+ channel agonists resu lts from their breakdown to a compound(s) that activates guanylate cyc lase.