Role of the NO/cGMP/K_ATP pathway in the protective effects of sildenafil against ethanol-induced gastric damage in rats
British Journal of Pharmacology (2008) 153, 721–727

Sildenafil is a selective inhibitor of cGMP-specific phosphodiesterase. Sildenafil, acting via NO-dependent mechanisms, prevents indomethacin-induced gastropathy. Activation of ATP-sensitive potassium channels (K_ATP) is involved in gastric defence.

Our objective was to evaluate the role of the NO/cGMP/K_ATP pathway in the protective effects of sildenafil against ethanol-induced gastric damage.

Sildenafil significantly reduced ethanol-induced gastric damage in rats. L-NAME alone, without L-arginine, significantly reversed the protection afforded by sildenafil. Inhibition of guanylate cyclase by ODQ completely abolished the gastric protective effect of sildenafil against ethanol-induced gastric damage. Glibenclamide alone reversed sildenafil's gastric protective effect. However, glibenclamide plus diazoxide did not alter the effects of sildenafil.

Sildenafil had a protective effect against ethanol-induced gastric damage through the activation of the NO/cGMP/K_ATP pathway.

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