Document Detail


Low-dose PGE2 mimics the duodenal secretory response to luminal acid in mice.
MedLine Citation:
PMID:  14764447     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Luminal exposure to concentrated acid, the most accepted physiological stimulus for duodenal bicarbonate secretion (DBS), cannot be used with in vitro preparations due to potential tissue damage. We thus examined whether exposure to PGE(2), a well-characterized physiological duodenal secretagogue, could mimic the effects of acid perfusion. DBS was measured in C57/BL mice by pH-stat/back-titration and measurement of total dissolved CO(2) concentration ([CO(2)](t)). Anion transport inhibitor DIDS, anion channel inhibitor 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), carbonic anhydrase inhibitor methazolamide, and nonselective cyclooxygenase inhibitor indomethacin were used to inhibit separate components of HCO(3)(-) secretory pathway. Baseline DBS was not altered by exposure to methazolamide (0.1 mM) but was slightly reduced by DIDS (0.5 mM). DBS and [CO(2)](t) increased after acid and PGE(2) exposure. DIDS (0.5 mM) and NPPB (0.2 mM) abolished acid-induced DBS increase. Methazolamide (0.1 mM) and DIDS inhibited acid-induced [CO(2)](t) increase. DIDS, NPPB, or methazolamide had little effect on DBS in response to high concentration PGE(2) (100 microg/ml). Low concentration PGE(2) (1 microg/ml) increased DBS that was inhibited by DIDS, NPPB, and methazolamide. Pretreatment with indomethacin (5 mg/kg) inhibited DBS induced by acid exposure but not by PGE(2). High-dose PGE(2) substantially increases DBS by a mechanism that appears to be different than secretory response to luminal acid perfusion. Secretory response to low-dose PGE(2), at least in terms of inhibitor profile, closely resembles secretion in response to perfusion of physiological acid concentrations and may be a useful stimulus for in vitro study of DBS in isolated mouse duodenum.
Authors:
Masahiko Hirokawa; Osamu Furukawa; Paul H Guth; Eli Engel; Jonathan D Kaunitz
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.     Date:  2004-02-05
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  286     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-05-10     Completed Date:  2004-06-10     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G891-8     Citation Subset:  IM    
Affiliation:
Center for Ulcer Research and Education: Digestive Diseases Research Center, Los Angeles 90073, USA.
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MeSH Terms
Descriptor/Qualifier:
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / pharmacology
Acids / metabolism*
Animals
Anions / metabolism
Bicarbonates / metabolism*
Biological Transport / drug effects
Carbonic Anhydrase Inhibitors / pharmacology
Dinoprostone / administration & dosage*
Dose-Response Relationship, Drug
Duodenum / drug effects*,  metabolism*
Ion Channels / antagonists & inhibitors
Male
Methazolamide / pharmacology
Mice
Mice, Inbred C57BL
Nitrobenzoates / pharmacology
Grant Support
ID/Acronym/Agency:
R01 DK-54221/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Acids; 0/Anions; 0/Bicarbonates; 0/Carbonic Anhydrase Inhibitors; 0/Ion Channels; 0/Nitrobenzoates; 107254-86-4/5-nitro-2-(3-phenylpropylamino)benzoic acid; 363-24-6/Dinoprostone; 53005-05-3/4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; 554-57-4/Methazolamide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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