Stimulation by sparkling water of gastroduodenal HCO3- secretion in rats.
BACKGROUND
We examined the effect of sparkling water on gastroduodenal HCO3- secretion in rats and investigated the factors involved in these responses.


METHODS
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-.
Sasaki
Yoko
Y
Division of Pathological Sciences, Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto, Japan.
Aihara
Eitaro
E
Ohashi
Yumi
Y
Okuda
Sayaka
S
Takasuka
Hironori
H
Takahashi
Kento
K
Takeuchi
Koji
K
D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000086:Acetazolamide / Q000494:pharmacology; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D002211:Capsaicin / Q000494:pharmacology; D002253:Carbonated Beverages / Q000633:toxicity*; D015232:Dinoprostone / Q000378:metabolism; D004386:Duodenum / Q000187:drug effects / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism*; D007213:Indomethacin / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014867:Water / Q000494:pharmacology*
D001639:Bicarbonates; D014867:Water; C039465:5-dimethylamiloride; D000584:Amiloride; D015232:Dinoprostone; D000086:Acetazolamide; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D002211:Capsaicin; D007213:Indomethacin