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Yoko Sasaki, Eitaro Aihara, Yumi Ohashi, Sayaka Okuda, Hironori Takasuka, Kento Takahashi, Koji Takeuchi
Med Sci Monit 2009; 15(12): BR349-356
We examined the effect of sparkling water on gastroduodenal HCO3- secretion in rats and investigated the factors involved in these responses.
Material and Method: Under urethane anesthesia, a chambered stomach or a proximal duodenal loop was superfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat.
Results: The amount of CO2 in sparkling water was about 7.2 g/L. The mucosal exposure with sparkling water increased the secretion of HCO3- in both the stomach and duodenum. The HCO3- response in the duodenum was partially inhibited by indomethacin, acetazolamide or sensory deafferentation and was totally abolished by the co-administration of the former two agents. By contrast, the response in the stomach was almost totally inhibited by acetazolamide and partially mitigated by indomethacin but not sensory deafferentation. DIDS [an inhibitor of the Cl-/HCO3- exchanger (AE) and the Na+-HCO3- cotransporter (NBC)] and DMA [an inhibitor of the Na+/H+ exchanger 1 (NHE1)] partially mitigated the HCO3- response in the duodenum but not the stomach. The mucosal application of sparkling water increased prostaglandin E2 content in these tissues.
Conclusions: Sparkling water stimulates HCO3- secretion in both the stomach and the duodenum, but the mechanisms involved differ in these two tissues; the response in the former is mainly due to the intracellular supply of HCO3- with the aid of carbonic anhydrase, while in the latter the response is dependent on the NHE1, AE and NBC, and is mediated by endogenous prostaglandins as well as capsaicin-sensitive afferent neurons, in addition to the intracellular supply of HCO3-.