Involvement of nitrosothiols, nitric oxide and voltage-gated K+ channels in photorelaxation of vascular smooth muscle.

The effects of nitrosothiol depleting compounds (p-hydroxymercuribenzoate, iodacetamide and ethacrynic acid), a guanylyl cyclase inhibitor (1H[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, ODQ) and nitric oxide (NO) scavenger agents (xanthine/xanthine oxidase and 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide; carboxy-PTIO) on light-induced photorelaxation in rat thoracic aorta were investigated. Photorelaxation responses were decreased in the presence of nitrosothiol depleting compounds suggesting S-nitrosothiols as the tissue source of the NO, whereas reduction in photorelaxation by the guanylyl cyclase inhibitor and NO scavenger agents indicates involvement of both NO and cGMP in photorelaxation. In addition the sensitivity of photorelaxation to the voltage-gated potassium channel (KV) inhibitor, 4-aminopyridine, indicates that photorelaxation is mediated via a NO/cGMP-dependent, and, perhaps, direct light, activation of KV channels.