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Vol. 301, Issue 2, 611-617, May 2002
Center for Ulcer Research and Education: Digestive Diseases
Research Center, Veterans Affairs Greater Los Angeles Healthcare
System, Department of Medicine, Digestive Diseases Division and Brain
Research Institute, University of California at Los Angeles, Los
Angeles, California (V.M., L.W., Y.T.); and Clayton Foundation
Laboratories for Peptide Biology, the Salk Institute for Biological
Studies, La Jolla, California (J.E.R., W.V.).
Peripheral CRF inhibits gastric emptying and stimulates colonic motor
function in rats. We investigated the role of CRF1
and CRF2 receptors in i.p. CRF-induced alterations of gut
transit in conscious mice using selective CRF1 and
CRF2 ligands injected i.p. Gastric emptying 2 h after
ingestion of a solid chow meal and colonic transit (time to expel a
bead inserted into the distal colon) were determined simultaneously.
Rat/human (r/h)CRF, which has CRF1 > CRF2
binding affinity, decreased distal colonic transit time at lower doses
(6-12 µg/kg) than those inhibiting gastric emptying (20-60
µg/kg). Ovine CRF, a preferential CRF1 receptor agonist
(6-60 µg/kg), reduced significantly the colonic transit time without
altering gastric emptying, whereas the selective CRF2
receptor agonists mouse urocortin II (20-60 µg/kg) and urocortin III
(120 µg/kg) inhibited significantly gastric emptying without modifying colonic transit. The CRF1/CRF2
receptor antagonist, astressin (30-120 µg/kg), dose
dependently prevented r/hCRF (20 µg/kg)-induced inhibition of gastric
emptying and reduction of colonic transit time. The selective
CRF1 receptor antagonists, NBI-27914
(C18H20Cl4N4C7H8O3S)
and CP-154,526
(butyl-[2,5-dimethyl-7-(2,4,6-trimethylphenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yl]ethylamine) (5-30 mg/kg), dose dependently blocked r/hCRF action on the colon without influencing the gastric response, whereas the CRF2
receptor antagonist, antisauvagine-30 (30-100 µg/kg), dose
dependently abolished r/hCRF-induced delayed gastric emptying and had
no effect on colonic response. These data show that i.p. r/hCRF-induced opposite actions on upper and lower gut transit in conscious mice are
mediated by different CRF receptor subtypes: the activation of
CRF1 receptors stimulates colonic propulsive activity,
whereas activation of CRF2 receptors inhibits gastric emptying.
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