Basolateral membrane mechanisms involved in ligustrazine-stimulated anion secretion in rat distal colon.
- Author:
Ying XING
1
;
Qiong HE
;
Jin-Xia ZHU
;
Hsiao-Chang CHAN
Author Information
1. Department of Physiology, Medical School, Zhengzhou University, Zhengzhou 450052.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Calcium Channel Blockers;
pharmacology;
Colon;
metabolism;
physiology;
Epithelial Cells;
metabolism;
Evoked Potentials;
drug effects;
In Vitro Techniques;
Intestinal Mucosa;
cytology;
metabolism;
Ion Transport;
drug effects;
Male;
Potassium Channels;
metabolism;
Pyrazines;
pharmacology;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2003;55(6):653-657
- CountryChina
- Language:English
-
Abstract:
The present study investigated the cellular mechanism underlying the effect of ligustrazine on the ion transport in rat distal colon using the short-circuit current (I(SC)) technique. In freshly isolated colonic strips, basolateral addition of ligustrazine stimulated a rise in I(SC), which was resistant to basolateral application of neuronal sodium channel blocker tetrodotoxin (TTX), but inhibited by 55.2% by basolateral pretreatment with prostaglandin inhibitor indomethacin. The ligustrazine-induced I(SC) increase was inhibited by apical application of Cl(-) channel blockers diphenylamine-2,2'-dicarboxylic acid (DPC) and glibenclamide. Basolaterally administered bumetanide, an inhibitor of Na(+)-K(+)-2 Cl(-) cotransporter, inhibited ligustrazine-evoked current increases by 85.2% and basolateral exposure to Ba(2+), a non-specific potassium channels blocker, and blocked the current by more than 90%, indicating that basolateral Na(+)-K(+)-2 Cl(-) cotransporter and K(+) channels played an important role in the effect of ligustrazine. The results suggested that ligustrazine could stimulate rat distal colon (-) secretion that is mediated by basolateral Na(+)-K(+)-2 Cl(-) cotransporter and K(+) channel.
