Abstract
The rebound contraction induced by electrical field stimulation (EFS) and nitric oxide (NO) donor, S-nitroso-L-cysteine (cysNO), were investigated in the longitudinal muscle of porcine gastric fundus (LM-PGF). Under the presence of atropine and guanethidine, cysNO and EFS produced sequential relaxation-contraction in LM-PGF. Tetrodotoxin abolished the EFS-induced response, while leaving the cysNO-induced one unaffected. A soluble guanylate cyclase inhibitor, lH-[1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one, inhibited both cysNO and EFS-induced biphasic response. A cGMP analogue only relaxed LM-PGF. A phosphodiesterase V inhibitor, zaprinast, prolonged the cysNO and the EFS-induced relaxation and inhibited the rebound contraction. The rebound contraction was inhibited by verapamil, an L-type Ca2+ channel blocker. The cysNO and the EFS-induced biphasic response were inhibited by ryanodine plus cyclopiazonic acid or by ruthenium red, a ryanodine-receptor blocker. LM-PGF was relaxed on exposure to caffeine and then produced a verapamil-sensitive rebound contraction during the washout period. CysNO and EFS did not induce the rebound contraction in the presence of caffeine. These results suggest that the NO-induced rebound contraction involves both Ca2+-release from the ryanodine-sensitive store and Ca2+-influx through L-type channels. Although the NO-induced biphasic response is dependent on cGMP, rapid removal of cGMP seems necessary for the rebound contraction.
