In:
American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 280, No. 2 ( 2001-02-01), p. G216-G221
Abstract:
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 HCO 3 − 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 ( J R ), indicating net HCO 3 − 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 ) and decreased net Cl − flux ( J net Cl ) accompanied by increases in short-circuit current ( I sc ), 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.
Type of Medium:
Online Resource
ISSN:
0193-1857
,
1522-1547
DOI:
10.1152/ajpgi.2001.280.2.G216
Language:
English
Publisher:
American Physiological Society
Publication Date:
2001
detail.hit.zdb_id:
1477329-6
SSG:
12
Permalink