The effect of nitric oxide donors and L-arginine on the gastric electrolyte barrier.

The potential difference across the stomach wall (PD) is determined by the gastric mucosal barrier. The decrease in the PD evoked by "the barrier breakers", e.g. aspirin, ethanol or bile acids is believed as a sensitive index of the mucosal damage. The effect of glyceryl trinitrate (GTN), isosorbide dinitrate (IDN) and molsidomine (MOL)--all exogenous donors of nitric oxide (NO), as well as L-arginine (L-ARG), which is a substrate for NO-synthase and Nomega-nitro-L-arginine (L-NNA), a non-selective NO synthase inhibitor on the gastric electrolyte barrier were studied against the gastric damage induced by ethanol. All NO donors given intragastrically alone caused only moderate, not significant changes in the PD and failed to affect the mucosal barrier, while L-NNA slightly decreased the PD. The NO donors and L-arginine applied as pretreatment prior to ethanol resulted in diminishing of its damaging action that was similar for all these drugs, while L-NNA intensified both the injury and the drop in the PD values caused by ethanol. In summary, our results showed the protective effect of endogenous nitric oxide from L-ARG and that originating from GTN, MOL and IDN on the gastric electrolyte barrier, supporting involvement of nitric oxide in the mechanism of gastric protection in the stomach.