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Mediation by CCK B receptors of the CCK‐evoked hyperaemia in rat gastric mucosa
Author(s) -
Heinemann Akos,
Jociĉ Milana,
HolzerPetsche Ulrike,
Pethö Gábor,
Peskar Brigitta M.,
Horwell David C.,
Holzer Peter
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb15064.x
Subject(s) - gastrin , endocrinology , cholecystokinin , medicine , receptor antagonist , tachykinin receptor , receptor , gastrointestinal hormone , cholecystokinin receptor , chemistry , gastric acid , antagonist , biology , stomach , peptide hormone , neuropeptide , secretion , substance p
1 Cholecystokinin octapeptide (CCK‐8) and gastrin‐17 augment gastric mucosal blood flow in the rat. The present study examined whether the gastric vasodilator effect of these peptides is mediated by CCK A or CCK B receptors. 2 Intravenous injection of CAM‐1481 (1 mg kg −1 ), a dipeptoid antagonist of CCK A receptors, or CAM‐1028, a dipeptoid CCK B receptor antagonist (1 mg kg −1 ), had no effect on basal gastric mucosal blood flow as determined by the clearance of hydrogen in urethane‐anaesthetized rats. 3 Intravenous infusion of CCK‐8 or gastrin‐17 (8–200 pmol min −1 ) increased gastric mucosal blood flow in a dose‐dependent fashion. The CCK B receptor antagonist, CAM‐1028, significantly attenuated the hyperaemic response to CCK‐8 and gastrin‐17 whereas the CCK A receptor antagonist, CAM‐1481, did not antagonize CCK‐8 but caused a slight attenuation of the vasodilator response to gastrin‐17. 4 The selectivity of the two antagonists was proved by the findings that CAM‐1028, but not CAM‐1481, inhibited gastric acid secretion evoked by CCK‐8 or gastrin‐17 (CCK B receptor assay) while CAM‐1481, but not CAM‐1028, inhibited the CCK‐8‐induced contraction of guinea‐pig isolated gall bladder strips (CCK A receptor assay). 5 These data show that the actions of CCK‐8 and gastrin‐17 to increase mucosal blood flow in the rat stomach are primarily mediated by CCK B receptors.