further demonstrated that the observed motor effects of vagal stimulation concerned generation of NO within the gastric wall. On another hand, VIP villain had supplier AG-1478 no influence on DMPP evoked citrulline increase. DMPPevoked VIP release wasn’t affected by L NNA. DISCUSSION In this study, we demonstrated that both VIP and nitric oxide get excited about the vagal regulation of gastric relaxation. Electrical stimulation of the trunk produced a response which was made up of a rapid transient relaxation accompanied by a late continuous relaxation and a phasic contraction. These responses were completely abolished by intraarterial infusion of a Ca2 free medium containing 1 mM EDTA or tetrodotoxin, indicating the involvement of neural mechanisms. Our studies also demonstrated that electrical vagal stimulation resulted in both gastric relaxation and contraction but optimal responses occurred at different wavelengths, indicating that these responses are mediated via different neural pathways and neurotransmitters. Triphasic responses to electrical nerve stimulation in the rat stomach have already been shown both in vitro and in vivo. Ito et al. 1 50 NO 0 confirmed a response using circular muscle strips obtained from embryonic rat stomach. Consistent with our results, they showed the first phase of fast relaxation, Retroperitoneal lymph node dissection the second phase of contraction and the 3rd phase of delayed relaxation were at a maximum at 2, 5 and 10 Hz, respectively. Lefebvre et al. reported that vagal stimulation produced a response which was consists of an instant relaxation, accompanied by a delayed relaxation and a rebound contraction. As T NNA notably antagonized the fast relaxation and enhanced the contraction without impacting the delayed relaxation, and as atropine inhibited the rebound contraction, the authors suggested that the next phase of contraction and the first phase of relaxation were mediated by acetylcholine and NO, respectively. c-Met kinase inhibitor Nevertheless, the mechanism for the 3rd phase of delayed relaxation was not addressed. To ensure the role of NO in the regulation of gastric leisure, we examined the effects of L NNA, a nitric oxide biosynthesis inhibitor. L NNA dramatically antagonized the primary stage of relaxation in reaction to vagal stimulation. The inhibitory effect of L NNA was somewhat prevented by the pre administration of L arginine but not by D arginine. These observations indicate that the fast relaxation in response to vagal stimulation was mediated by the release of NO. Methylene Blue is reported to be described as a selective inhibitor of soluble guanylate cyclase, the proposed site of action of NO. Much like L NNA, Methylene Blue completely antagonized the primary phase of relaxation and enhanced the second phase of contraction. The 2nd phase of contraction in reaction to vagal stimulation was dramatically antagonized by atropine, indicating mediation by acetylcholine release from the gastric myenteric plexus.