Abstract
We examined the effect of nicotine on the release of endogenous noradrenaline(NA)from the isolated, vascularly perfused rat stomach.The stomach was perfused via the coeliac artery with Krebs−Ringer solution containing 10 μM pargyline at a constant flow rate of 4 ml per minute.Nicotine was once applied in the perfusion medium for 2 min.Nicotine(10-6−10-4M)evoked NA release in a concentration−dependent manner.The nicotine(3×10-5M)−evoked NA release was abolished by hexamethonium and tetrodotoxin.Diltiazem and isradipine [blockers of L−type voltage−activated calcium channel(VACC)] and ω−conotoxin GVIA(a blocker of N−type VACC)also abolished this nicotine−evoked NA release.Previously we reported that N−type, but not L−type, VACCs are located on the gastric postganglionic sympathetic nerve terminals, since the NA release evoked by electrical stimulation of periarterial nerves around the left gastric artery(postganglionic sympathetic nerves)was abolished by ω−conotoxin GVIA, but not by diltiazem(Yokotani et al., Jpn.J.Pharmacol.78, 75−77, 1998).From these results, it was suggested that nicotine activates nicotinic acetylcholine receptors located on the sympathetic ganglia, thereby evoking NA release by activation of L−type VACC located on the gastric sympathetic ganglia and N−type VACC probably located on the sympathetic nerve terminals in the rat stomach.
