Effect of E-coli heat-stable enterotoxin on colonic transport in guanylyl cyclase C receptor-deficient mice
Effect of E-coli heat-stable enterotoxin on colonic transport in guanylyl cyclase C receptor-deficient mice
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DOI:
10.1152/ajpgi.2001.280.2.g216
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发表时间:
2001-02-01
影响因子:
4.5
通讯作者:
Giannella, RA
中科院分区:
文献类型:
--
作者:
Charney, AN;Egnor, RW;Giannella, RA
We studied the functional importance of the colonic guanylyl cyclase C (GCC) receptor in GCC receptor-deficient mice. Mice were anesthetized with pentobarbital sodium, and colon segments were studied in Ussing chambers in HCO3- Ringer under short-circuit conditions. Receptor-deficient mouse proximal colon exhibited similar net Na+ absorption, lower net Cl- absorption, and a negative residual ion flux (JR), indicating net HCO3- absorption compared with that in normal mice. In normal mouse proximal colon, mucosal addition of 50 nM Escherichia coli heat-stable enterotoxin (STa) increased the serosal-to-mucosal flux of Cl- (J(s-->m)(Cl) Cl) and decreased net Cl- flux (J(net)(Cl)) accompanied by increases in short-circuit current (Isc), potential difference (PD), and tissue conductance (G). Serosal STa had no effect. In distal colon neither mucosal nor serosal STa affected ion transport. In receptor-deficient mice, neither mucosal nor serosal 500 nM STa affected electrolyte transport in proximal or distal colon. In these mice, 1 mM 8-bromo-cGMP produced changes in proximal colon J(s-->m)(Cl) and J(net)(Cl), I-sc, PD, G, and J(R) similar to mucosal STa addition in normal mice. We conclude that the GCC receptor is necessary in the mouse proximal colon for a secretory response to mucosal STa.