Document Detail


Chloride secretion in response to guanylin in colonic epithelial from normal and transgenic cystic fibrosis mice.
MedLine Citation:
PMID:  7518307     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Guanylin, a 15 amino acid endogenous gut peptide, increased the short circuit current (SCC) in the epithelium of the mouse colon, but only when applied to the apical and not the basolateral surface. 2. By use of selective blockers of epithelial ion transport and modification of the bathing solution, it was concluded that guanylin increased electrogenic chloride secretion but also had a minor effect on electrogenic sodium absorption. In addition there were small residual currents which remained unresolved. 3. The threshold concentration of guanylin causing a SCC increase was less than 50 nM, but at concentrations 40 times greater no indication of a maximally effective concentration was found. 4. Two guanylin isomers with the same amino acid sequence but with the disulphide bridges joined in an alternate fashion showed no activity. Thus only guanylin with the greatest structural homology to heat stable enterotoxin (STa) showed biological activity. 5. The action of guanylin was virtually eliminated in colonic epithelia from transgenic cystic fibrosis (CF) mice. As these animals lack the chloride channel coded by the CF gene sequence, it is likely that the final effector process in murine colonic epithelia involves the CFTR (cystic fibrosis transmembrane conductance regulator) chloride channel. 6. Opportunistic infections of the gut generating STa lead to diarrhoeal conditions via an action of the toxin on apical guanylin receptors. Thus, as discussed, the CF heterozygote may have a genetic advantage in this circumstance.
Authors:
A W Cuthbert; M E Hickman; L J MacVinish; M J Evans; W H Colledge; R Ratcliff; P W Seale; P P Humphrey
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  112     ISSN:  0007-1188     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  1994 May 
Date Detail:
Created Date:  1994-08-16     Completed Date:  1994-08-16     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  31-6     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Glaxo Institute of Applied Pharmacology, Cambridge.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Bacterial Toxins / pharmacology
Chloride Channels / drug effects,  genetics,  metabolism
Chlorides / metabolism*
Colon / drug effects,  metabolism
Cystic Fibrosis / genetics,  metabolism*
Cystic Fibrosis Transmembrane Conductance Regulator
Enterotoxins / pharmacology
Epithelium / drug effects,  metabolism
Gastrointestinal Hormones*
Heterozygote
Intestinal Mucosa / drug effects,  metabolism*
Isomerism
Membrane Proteins / drug effects,  metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Molecular Sequence Data
Natriuretic Peptides
Peptides / pharmacology*
Grant Support
ID/Acronym/Agency:
//Wellcome Trust
Chemical
Reg. No./Substance:
0/Bacterial Toxins; 0/Chloride Channels; 0/Chlorides; 0/Enterotoxins; 0/Gastrointestinal Hormones; 0/Membrane Proteins; 0/Natriuretic Peptides; 0/Peptides; 0/heat stable toxin (E coli); 126880-72-6/Cystic Fibrosis Transmembrane Conductance Regulator; 140653-38-9/guanylin
Comments/Corrections

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


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