Segmental heterogeneity of electrogenic secretions in human ascending colon and rectum.
OBJECTIVE
We have attempted to ascertain putative segmental differences in the secretory responses of the human ascending colon and rectum.


METHODS
From the mucosal biopsy samples of two segments, the short-circuit current (I(sc)) and tissue resistance (R(te)) were compared under control conditions, as well as after the induction of secretion, using a modified Ussing chamber. We also performed semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to detect and quantify transport proteins.


RESULTS
The spontaneous I(sc) in the ascending colon was found to be greater than that in the rectum (P<0.01), whereas isobutylmethylxanthine/forskolin and carbachol (CCh) induced a greater rise in I(sc) in the rectum than in the ascending colon (P<0.05). When coupled with indomethacin pretreatment, the increase in Delta I(sc) after the addition of CCh and forskolin was significant as compared to that observed without pretreatment (P<0.05). However, in the rectum, the secretory response to CCh and forskolin was abolished to a significant degree by indomethacin (P<0.05). Moreover, these indomethacin-induced changes were reversed by the addition of PGE2. Upon semiquantitative RT-PCR analysis, the amounts of cystic fibrosis transmembrane regulator, KCNQ1, and CLCA1 mRNAs were not found to be different between the two segments.


CONCLUSIONS
There was a clear segmental heterogeneity with regard to electrogenic secretion in the human colon, and this difference can be explained by differences in the ascending colon and rectum.
Park
Jung Ho
JH
Department of Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, 135-710, South Korea.
Rhee
Poong-Lyul
PL
Lee
Jun Haeng
JH
Kim
Jae Jun
JJ
Rhee
Jong Chul
JC
Kim
Sung Joon
SJ
Lee
Jiyeon
J
D015056:1-Methyl-3-isobutylxanthine / Q000493:pharmacokinetics; D002217:Carbachol / Q000493:pharmacokinetics; D018118:Chloride Channels / Q000235:genetics / Q000378:metabolism; D005576:Colforsin / Q000493:pharmacokinetics; D003106:Colon / Q000378:metabolism*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics / Q000378:metabolism; D015232:Dinoprostone / Q000493:pharmacokinetics; D004587:Electrophoresis, Agar Gel; D004594:Electrophysiology; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D017136:Ion Transport; D051657:KCNQ1 Potassium Channel / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012007:Rectum / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction
C492109:CLCA1 protein, human; D018118:Chloride Channels; D051657:KCNQ1 Potassium Channel; C496909:KCNQ1 protein, human; D012333:RNA, Messenger; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D005576:Colforsin; D002217:Carbachol; D015232:Dinoprostone; D015056:1-Methyl-3-isobutylxanthine