Document Detail

Appearance of segmental discrepancy of anion transport in rat distal colon.
MedLine Citation:
PMID:  17666794     Owner:  NLM     Status:  MEDLINE    
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).
Hong Xue; Yue Min Tian; Ming Yan; Ning Yang; Xin Chen; Ying Xing; Jin Xia Zhu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biological & pharmaceutical bulletin     Volume:  30     ISSN:  0918-6158     ISO Abbreviation:  Biol. Pharm. Bull.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-08-01     Completed Date:  2007-09-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9311984     Medline TA:  Biol Pharm Bull     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  1407-11     Citation Subset:  IM    
Department of Physiology, Basic Medical College, Capital Medical University, Beijing 100069, China.
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MeSH Terms
Adenylate Cyclase / metabolism
Anions / metabolism
Biological Transport, Active / physiology
Colon / metabolism*
Cyclic AMP / physiology
Cystic Fibrosis Transmembrane Conductance Regulator / biosynthesis,  genetics
Enzyme Activators / pharmacology
Forskolin / pharmacology
Gene Expression / physiology
Glyburide / pharmacology
RNA, Messenger / biosynthesis,  genetics
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction
Sodium-Potassium-Chloride Symporters / biosynthesis,  genetics
Reg. No./Substance:
0/Anions; 0/Enzyme Activators; 0/RNA, Messenger; 0/Sodium-Potassium-Chloride Symporters; 0/sodium-potassium-chloride cotransporter 1 protein; 10238-21-8/Glyburide; 126880-72-6/Cystic Fibrosis Transmembrane Conductance Regulator; 60-92-4/Cyclic AMP; 66428-89-5/Forskolin; EC Cyclase

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