The involvement of multiple K+ channels in photorelaxation in mouse gastric fundus

Abstract

Purpose:Our previous study has indicated that mouse gastric fundus has a photosensitive material store and nitric oxide (NO), or a related compound, is responsible for the photorelaxation.However, the mechanism underlying the photorelaxation induced by ultraviolet-light is unkown.This study addresses the question whether potassium ($K^+$) channels are involved in the ultraviolet light-induced photorelaxation of mouse isolated methacholine-contracted gastric fundal strips. Methods:We tested the effects of $K^+$ channel blockers on photorelaxation of mouse isolated methacholine-contracted gastric fundal strips. Results:Photorelaxation responses were inhibited by charybdotoxin (0.23 $mu$M), a blocker of large conductance $Ca^{2+}$ - activated $K^+$ channels, and apamin (1$mu$M), a blocker of small conductance $Ca^{2+}$ - activated $K^+$ channels.Non-specific $Ca^{2+}$ - activated $K^+$ channel blocker tetraethylammonium (10 $mu$M to 1 mM) also inhibited the photorelaxation in a concentration-dependent manner.4-aminopyridine (10 $mu$M and 100 $mu$M), a voltage-gated $K^+$ channel blocker, slightly reduced the photorelaxation.ATP-sensitive $K^+$ channel blocker glibenclamide (0.1 nM to 1$mu$M) significantly reduced photorelaxant responses and the inhibitory effect of glibenclamide on the photorelaxation was prevented by cromakalim (100 $mu$M), an opener of ATP-sensitive $K^+$ channels. Conclusion:These results suggest that activation of the small or large conductance $Ca^{2+}$ - activated $K^+$ channels, voltage-gated $K^+$ channels and ATP-sensitive $K^+$ channels may be part of mechanism underlying photorelaxation in mouse gastric fundal strips, and activation of $K^+$ channels may due to cyclic GMP and/or direct ultraviolet light-dependent mechanism.Furthermore, mouse gastric fundus as non-vascular smooth muscle is a useful tissue to elucidate the mechanisms of photorelaxation.