Mucosal nitric oxide is not responsible for the hemodynamic changes induced by nicotine in rat stomachs

Abstract

It has been shown that chronic nicotine treatment decreases gastric mucosal blood flow (GMBF). The mechanism for this action is still not defined. In this study, nicotine treatment (5, 25 or 50 μg/ml drinking water) for 10 days dose dependently reduced the GMBF and volume of hemoglobin but increased ethanol-induced gastric damage. These effects were potentiated by N(ω)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, L-arginine but not the D-analog restored the actions of L-NAME, indicating that the selective action of L-NAME. However, the potentiating actions of L-NAME were significantly attenuated in the nicotine-pretreated rats. When the basal mucosal NO synthase (both iNOS and cNOS) activity and its second messenger cyclic GMP levels were measured, no difference was found between the nicotine and the non-nicotine groups. Furthermore, high dose of L-arginine could not reverse the action of nicotine. These findings suggest that the adverse action of chronic nicotine treatment on GMBF and lesion formation is probably mediated through a NO independent mechanism.