ArticleProceedings of the National Academy of Sciences of the United States of America2009
Duodenal acidity "sensing" but not epithelial HCO3- supply is critically dependent on carbonic anhydrase II expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 37 citations in OpenAlex.
- Bicarbonate secretion and acid/base sensing by the intestine.Pflugers Archiv : European journal of physiology · 2024Review
- Carbonic Anhydrases II and IX in Non-ampullary Duodenal Adenomas and Adenocarcinoma.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Article
- Human Enteroids as a Model of Upper Small Intestinal Ion Transport Physiology and Pathophysiology.Gastroenterology · 2016Article
- Carbonic anhydrase II binds to and increases the activity of the epithelial sodium-proton exchanger, NHE3.American journal of physiology. Renal physiology · 2015Article
- Emerging concepts in liver graft preservation.World journal of gastroenterology · 2015Review
- The distinct roles of anion transporters Slc26a3 (DRA) and Slc26a6 (PAT-1) in fluid and electrolyte absorption in the murine small intestine.Pflugers Archiv : European journal of physiology · 2014Article
- Essential role of the electroneutral Na+-HCO3- cotransporter NBCn1 in murine duodenal acid-base balance and colonic mucus layer build-up in vivo.The Journal of physiology · 2013Article
- Rescue of epithelial HCO3- secretion in murine intestine by apical membrane expression of the cystic fibrosis transmembrane conductance regulator mutant F508del.The Journal of physiology · 2012Article
- Cell-specific effects of luminal acid, bicarbonate, cAMP, and carbachol on transporter trafficking in the intestine.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- The electroneutral Na⁺:HCO₃⁻ cotransporter NBCn1 is a major pHi regulator in murine duodenum.The Journal of physiology · 2012Article
- Loss of downregulated in adenoma (DRA) impairs mucosal HCO3(-) secretion in murine ileocolonic inflammation.Inflammatory bowel diseases · 2012Article
- Luminal chemosensing in the duodenal mucosa.Acta physiologica (Oxford, England) · 2011Review
- Duodenal chemosensing and mucosal defenses.Digestion · 2011Article
- Physiological relevance of cell-specific distribution patterns of CFTR, NKCC1, NBCe1, and NHE3 along the crypt-villus axis in the intestine.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Microanatomy of the intestinal lymphatic system.Annals of the New York Academy of Sciences · 2010Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbonic anhydrase (CA) is strongly expressed in the duodenum and has been implicated in a variety of physiological functions including enterocyte HCO(3)(-) supply for secretion and the "sensing" of luminal acid and CO(2). Here, we report the physiological role of the intracellular CAII isoform involvement in acid-, PGE(2,) and forskolin-induced murine duodenal bicarbonate secretion (DBS) in vivo. CAII-deficient and WT littermates were studied in vivo during isoflurane anesthesia. An approximate 10-mm segment of the proximal duodenum with intact blood supply was perfused under different experimental conditions and DBS was titrated by pH immediately. Two-photon confocal microscopy using the pH-sensitive dye SNARF-1F was used to assess duodenocyte pH(i) in vivo. After correction of systemic acidosis by infusion of isotonic Na(2)CO(3), basal DBS was not significantly different in CAII-deficient mice and WT littermates. The duodenal bicarbonate secretory response to acid was almost abolished in CAII-deficient mice, but normal to forskolin- or 16,16-dimethyl PGE(2) stimulation. The complete inhibition of tissue CAs by luminal methazolamide and i.v. acetazolamide completely blocked the response to acid, but did not significantly alter the response to forskolin. While duodenocytes acidified upon luminal perfusion with acid, no significant pH(i) change occurred in CAII-deficient duodenum in vivo. The results suggest that CA II is important for duodenocyte acidification by low luminal pH and for eliciting the acid-mediated HCO(3)(-) secretory response, but is not important in the generation of the secreted HCO(3)(-) ions.
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