Nitric oxide released from luminal S-nitroso-N-acetylcysteine increases gastric mucosal blood flow

• Grant number: 15/03428-7
• Support Opportunities: Regular Research Grants - Publications - Scientific article
• Start date: May 01, 2015
• End date: October 31, 2015
• Field of knowledge: Physical Sciences and Mathematics - Chemistry - Physical-Chemistry
• Principal Investigator: Marcelo Ganzarolli de Oliveira
• Grantee: Marcelo Ganzarolli de Oliveira
• Host Institution: Instituto de Química (IQ). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

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 ¼M 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 ¼M and 12 mM) spontaneously released NO at 37 °C at a constant rate of 0.3 or 14 nmol·mL1·min1, respectively, while NaNO2 (12 mM) released NO at a rate of 0.06 nmol·mL1·min1 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. (AU)