Nitric Oxide Released from Luminal S-Nitroso-N-Acetylcysteine Increases Gastric Mucosal Blood Flow

Molecules

Gabriela F. P. de Souza¹  Patricia Taladriz-Blanco¹  Lໜio A. Velloso²  Marcelo G. de Oliveira¹ 

[1] Institute of Chemistry, University of Campinas, UNICAMP, CP 6154, Campinas, SP 13083-970, Brazil; E-Mails:;Faculty of Medical Sciences, University of Campinas, UNICAMP, CP, Campinas, SP 13084-970, Brazil; E-Mail:

关键词: nitric oxide;    S-nitroso-N-acetylcysteine;    gastric blood flow;    vasodilation;   

DOI  :  10.3390/molecules20034109

来源: mdpi

【 摘 要 】

Nitric oxide (NO)-mediated vasodilation plays a key role in gastric mucosal defense, and NO-donor drugs may protect against diseases associated with gastric mucosal blood flow (GMBF) deficiencies. In this study, we used the ex vivo gastric chamber method and Laser Doppler Flowmetry to characterize the effects of luminal aqueous NO-donor drug S-nitroso-N-acetylcysteine (SNAC) solution administration compared to aqueous NaNO₂ and NaNO₃ solutions (pH 7.4) on GMBF in Sprague-Dawley rats. SNAC solutions (600 μM and 12 mM) led to a rapid threefold increase in GMBF, which was maintained during the incubation of the solutions with the gastric mucosa, while NaNO₂ or NaNO₃ solutions (12 mM) did not affect GMBF. SNAC solutions (600 μM and 12 mM) spontaneously released NO at 37 °C at a constant rate of 0.3 or 14 nmol·mL⁻¹·min⁻¹, respectively, while NaNO₂ (12 mM) released NO at a rate of 0.06 nmol·mL⁻¹·min⁻¹ and NaNO₃ (12 mM) did not release NO. These results suggest that the SNAC-induced GMBF increase is due to their higher rates of spontaneous NO release compared to equimolar NaNO₂ solutions. Taken together, our data indicate that oral SNAC administration is a potential approach for gastric acid-peptic disorder prevention and treatment.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.