pH threshold for human duodenal bicarbonate secretion and diffusion of CO2

Feitelberg, SP; Hogan, D. L.; Koss, MA; Isenberg, J. I.

doi:10.1016/0016-5085(92)70020-c

Cited by 7 publications

(9 citation statements)

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“…To explain this apparent paradox, we hypothesized that the diminished HCO 3 Ϫ exit from the epithelial cells associated with CFTR dysfunction increases cellular [HCO 3 Ϫ ] and hence enhances buffering of cellular H ϩ . Because HCO 3 Ϫ uptake or accumulation into the epithelial cells occurs before DBS (3,11), inhibition of CFTR should augment cellular [HCO 3 Ϫ ] and, hence, buffering power. This concept is supported by our observation that the Cl Ϫ channel inhibitor 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) alkalinizes epithelial cells and reduces cellular acidification and injury due to luminal acid, even though NPPB inhibits acid-induced DBS (4).…”

mentioning

confidence: 99%

A novel small molecule CFTR inhibitor attenuates HCO₃⁻ secretion and duodenal ulcer formation in rats

Akiba¹,

Jung²,

Ouk³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ϫ ) secretion (DBS). Although impaired DBS is observed in CF mutant mice and in CF patients, which would predict increased ulcer susceptibility, duodenal injury is rarely observed in CF patients and is reduced in CF mutant mice. To explain this apparent paradox, we hypothesized that CFTR dysfunction increases cellular [HCO 3 Ϫ ] and buffering power. To further test this hypothesis, we examined the effect of a novel, potent, and highly selective CFTR inhibitor, CFTR inh-172, on DBS and duodenal ulceration in rats. DBS was measured in situ using a standard loop perfusion model with a pH stat under isoflurane anesthesia. Duodenal ulcers were induced in rats by cysteamine with or without CFTR inh-172 pretreatment 1 h before cysteamine. Superfusion of CFTR inh-172 (0.1-10 M) over the duodenal mucosa had no effect on basal DBS but at 10 M inhibited acid-induced DBS, suggesting that its effect was limited to CFTR activation. Acid-induced DBS was abolished at 1 and 3 h and was reduced 24 h after treatment with CFTRinh-172, although basal DBS was increased at 24 h. CFTR inh-172 treatment had no effect on gastric acid or HCO 3 Ϫ secretion. Duodenal ulcers were observed 24 h after cysteamine treatment but were reduced in CFTR inh-172-pretreated rats. CFTRinh-172 acutely produces CFTR dysfunction in rodents for up to 24 h. CFTR inhibition reduces acid-induced DBS but also prevents duodenal ulcer formation, supporting our hypothesis that intracellular HCO 3 Ϫ may be an important protective mechanism for duodenal epithelial cells.

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confidence: 99%

A novel small molecule CFTR inhibitor attenuates HCO₃⁻ secretion and duodenal ulcer formation in rats

Akiba¹,

Jung²,

Ouk³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In the proximal duodenum, CO 2 is produced when gastric acid is neutralized by HCO 3 -secreted from the surface epithelial cells, resulting in a marked increase in luminal PCO 2 (Rune et al, 1969;Feitelberg et al, 1992). Then, CO 2 generated in the lumen diffuses into the epithelial cells, where it is converted into H + and HCO 3 -by CA, and by so doing contributes to the intracellular supply of HCO 3 -in this tissue (Simon and Gutknecht, 1980).…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, it is also known that the proximal duodenum is exposed to an extreme elevation of PCO 2 because of the continuous mixture of secreted HCO 3 -with gastric acid (Rune et al, 1969;Feitelberg et al, 1992). Simon and Gutknecht (1980) reported that luminal CO 2 diffused into the duodenal epithelial cells, where it was converted into carbonic acid, then dissociated into H + and HCO 3 -by the catalysis of CA.…”

Section: Introductionmentioning

confidence: 98%

Stimulatory effect of Coca-ColaTM on gastroduodenal HCO3− secretion in rats

et al. 2007

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We examined the effect of various carbonated beverages, especially Coca-Cola, on the HCO3- secretion in the rat stomach and duodenum. Under urethane anaesthesia, a chambered stomach or a proximal duodenal loop was perfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. The amount of CO2 contained in these beverages was about 4-7 g/mL. Coca-Cola topically applied to the mucosa for 10 min significantly increased the HCO3- secretion in both the stomach and the duodenum. The HCO3- response in the duodenum was totally abolished by indomethacin and also partially inhibited by acetazolamide, an inhibitor of carbonic anhydrase. Likewise, the response in the stomach was also markedly inhibited by either acetazolamide or indomethacin. The mucosal application of Coca-Cola increased the PGE2 contents in both the stomach and the duodenum. Other carbonated beverages, such as sparkling water, Fanta Grape or cider, also increased the HCO3- secretion in these tissues. These results suggest that Coca-Cola induces HCO3- secretion in both the stomach and the duodenum, and these responses may be attributable to both the intracellular supply of HCO3- generated via carbonic anhydrase, and endogenous PGs, probably related to the acidic pH of the solution.

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“…However, during HCO 3 − secretion, the dissolved CO 2 concentration can accumulate to a significant concentration. Intestinal values of the partial pressure of carbon dioxide, P CO2 , (95-680 mmHg) (16,17) are significantly higher than atmospheric P CO2 or gastric P CO2 levels (18,19), 0.3 mmHg and 38 mmHg, respectively (Table I). The intestinal P CO2 values from dogs show that P CO2 nearly doubles in the fed state, due to the increased concentration of HCO 3 − secreted during digestion.…”

Section: Introductionmentioning

confidence: 97%

Exploration of Intestinal Calcium Precipitation as a Barrier to Absorption at High Calcium Doses

et al. 2008

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pH threshold for human duodenal bicarbonate secretion and diffusion of CO2

Cited by 7 publications

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A novel small molecule CFTR inhibitor attenuates HCO₃⁻ secretion and duodenal ulcer formation in rats

A novel small molecule CFTR inhibitor attenuates HCO₃⁻ secretion and duodenal ulcer formation in rats

Stimulatory effect of Coca-ColaTM on gastroduodenal HCO3− secretion in rats

Exploration of Intestinal Calcium Precipitation as a Barrier to Absorption at High Calcium Doses

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pH threshold for human duodenal bicarbonate secretion and diffusion of CO2

Cited by 7 publications

References 0 publications

A novel small molecule CFTR inhibitor attenuates HCO3− secretion and duodenal ulcer formation in rats

A novel small molecule CFTR inhibitor attenuates HCO3− secretion and duodenal ulcer formation in rats

Stimulatory effect of Coca-ColaTM on gastroduodenal HCO3− secretion in rats

Exploration of Intestinal Calcium Precipitation as a Barrier to Absorption at High Calcium Doses

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A novel small molecule CFTR inhibitor attenuates HCO₃⁻ secretion and duodenal ulcer formation in rats

A novel small molecule CFTR inhibitor attenuates HCO₃⁻ secretion and duodenal ulcer formation in rats