Document Detail


Duodenal acidity "sensing" but not epithelial HCO3- supply is critically dependent on carbonic anhydrase II expression.
MedLine Citation:
PMID:  19622732     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Markus Sjöblom; Anurag Kumar Singh; Wen Zheng; Jian Wang; Bi-guang Tuo; Anja Krabbenhöft; Brigitte Riederer; Gerolf Gros; Ursula Seidler
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-21
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  106     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-08-11     Completed Date:  2009-08-26     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  13094-9     Citation Subset:  IM    
Affiliation:
Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover 30625, Germany.
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MeSH Terms
Descriptor/Qualifier:
16,16-Dimethylprostaglandin E2 / pharmacology
Acetazolamide / pharmacology
Animals
Bicarbonates / metabolism*
Carbon Dioxide / metabolism
Carbonic Anhydrase II / antagonists & inhibitors,  physiology*
Duodenum / metabolism*
Forskolin / pharmacology
Hydrogen-Ion Concentration
Methazolamide / pharmacology
Mice
Mice, Inbred C57BL
Chemical
Reg. No./Substance:
0/Bicarbonates; 124-38-9/Carbon Dioxide; 39746-25-3/16,16-Dimethylprostaglandin E2; 554-57-4/Methazolamide; 59-66-5/Acetazolamide; 66428-89-5/Forskolin; EC 4.2.1.-/Carbonic Anhydrase II
Comments/Corrections

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