Linked Life Data

17666794

Source:http://linkedlifedata.com/resource/pubmed/id/17666794

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-8-1
pubmed:abstractText
The present study investigated the segmental discrepancy of the rat distal colonic anion transport induced by luminal forskolin and the possible underlying mechanisms using short-circuit current recording technique and comparative quantity real-time PCR analysis. Forskolin-induced I(SC) in the segment next to lymph node (DC(1)) and the segment 4 cm away from lymph node (DC(4)) were 4.09+/-0.66 muA/cm(2) and 18.84+/-3.18 muA/cm(2) (n=13), respectively, which were blocked by luminal Cl(-) channel blocker, glybenclamide (1 mM) (n=5, p<0.01), as well as removal of extracellular Cl(-) and HCO(3)(-) in both DC(1) and DC(4) (n=5, p<0.001). Furthermore luminal pretreatment with K(+) blockers, TEA (5 mM) and glybenclamide (100 muM) didn't affect forskolin and bumetanide-enhanced I(SC). Reducing serosal Cl(-) concentration increased forskolin-induced I(SC) by 90% in DC(1) but decreased forskolin-induced I(SC) in DC(4) by 50%. Furthermore, pretreatment with serosal bumetanide, an inhibitor of Na(+)-K(+)-2Cl(-) cotransporter, enhanced forskolin-induced I(SC) by 87% in DC(1), from 4.09+/-0.66 muA/cm(2) to 7.65+/-0.53 muA/cm(2) (n=6, p<0.01), but inhibited forskolin-induced I(SC) by 50% in DC(4), from 29.19+/-4.51 muA/cm(2) to 15.06+/-4.10 muA/cm(2) (n=6, p<0.05). Pretreatment with luminal amiloride (10 muM), an inhibitor of ENaC, and serosal 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) (200 muM), an inhibitor of NBC, significantly inhibited the forskolin-induced I(SC) in DC(1) (n=6, p<0.05), but not in DC(4). Real-time PCR analysis did not show the significant differences between the two segments in the expression amounts of CFTR and NKCC mRNAs, however the expression of NBC mRNA in DC(4) was significantly higher than that in DC(1). In conclusion, the rat distal colon manifests a segmental discrepancy in anion transport stimulated by luminal forskolin. HCO(3)(-) might be predominantly involved in the forskolin-induced anion secretion in DC(1), but Cl(-) might be the main component of the anion secretion in DC(4).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0918-6158
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1407-11
pubmed:meshHeading
pubmed-meshheading:17666794-Adenylate Cyclase, pubmed-meshheading:17666794-Animals, pubmed-meshheading:17666794-Anions, pubmed-meshheading:17666794-Biological Transport, Active, pubmed-meshheading:17666794-Colon, pubmed-meshheading:17666794-Cyclic AMP, pubmed-meshheading:17666794-Cystic Fibrosis Transmembrane Conductance Regulator, pubmed-meshheading:17666794-Enzyme Activators, pubmed-meshheading:17666794-Forskolin, pubmed-meshheading:17666794-Gene Expression, pubmed-meshheading:17666794-Glyburide, pubmed-meshheading:17666794-Male, pubmed-meshheading:17666794-RNA, Messenger, pubmed-meshheading:17666794-Rats, pubmed-meshheading:17666794-Rats, Sprague-Dawley, pubmed-meshheading:17666794-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17666794-Sodium-Potassium-Chloride Symporters
pubmed:year
2007
pubmed:articleTitle
Appearance of segmental discrepancy of anion transport in rat distal colon.
pubmed:affiliation
Department of Physiology, Basic Medical College, Capital Medical University, Beijing 100069, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't