Mediation by CCK(B) receptors of the CCK-evoked hyperaemia in rat gastric mucosa

A. Heinemann, M. Jocic, U. Holzer-Petsche, G. Pethő, B. M. Peskar, D. C. Horwell, P. Holzer

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)2274-2278
Number of pages5
JournalBritish Journal of Pharmacology
Volume116
Issue number4
Publication statusPublished - 1995

Fingerprint

Cholecystokinin B Receptor
Sincalide
Hyperemia
Gastric Mucosa
Cholecystokinin A Receptor
Stomach
Vasodilator Agents
Gastric Acid
Urethane
Intravenous Infusions
Intravenous Injections
gastrin 17
Hydrogen
Guinea Pigs
Urinary Bladder
Peptides
CAM 1481
PD 135158

Keywords

  • CAM-1028
  • CAM-1481
  • CCK receptor antagonists
  • CCK receptors
  • CCK(A) receptors
  • CCK(B) receptors
  • Cholecystokinin (CCK)
  • Cholecystokinin octapeptide (CCK-8)
  • Gall bladder contraction
  • Gastric acid secretion
  • Gastric mucosal blood flow
  • Gastrin
  • Gastrin-17
  • Hyperaemia
  • Vasodilatation

ASJC Scopus subject areas

  • Pharmacology

Cite this

Heinemann, A., Jocic, M., Holzer-Petsche, U., Pethő, G., Peskar, B. M., Horwell, D. C., & Holzer, P. (1995). Mediation by CCK(B) receptors of the CCK-evoked hyperaemia in rat gastric mucosa. British Journal of Pharmacology, 116(4), 2274-2278.

Mediation by CCK(B) receptors of the CCK-evoked hyperaemia in rat gastric mucosa. / Heinemann, A.; Jocic, M.; Holzer-Petsche, U.; Pethő, G.; Peskar, B. M.; Horwell, D. C.; Holzer, P.

In: British Journal of Pharmacology, Vol. 116, No. 4, 1995, p. 2274-2278.

Research output: Contribution to journalArticle

Heinemann, A, Jocic, M, Holzer-Petsche, U, Pethő, G, Peskar, BM, Horwell, DC & Holzer, P 1995, 'Mediation by CCK(B) receptors of the CCK-evoked hyperaemia in rat gastric mucosa', British Journal of Pharmacology, vol. 116, no. 4, pp. 2274-2278.
Heinemann A, Jocic M, Holzer-Petsche U, Pethő G, Peskar BM, Horwell DC et al. Mediation by CCK(B) receptors of the CCK-evoked hyperaemia in rat gastric mucosa. British Journal of Pharmacology. 1995;116(4):2274-2278.
Heinemann, A. ; Jocic, M. ; Holzer-Petsche, U. ; Pethő, G. ; Peskar, B. M. ; Horwell, D. C. ; Holzer, P. / Mediation by CCK(B) receptors of the CCK-evoked hyperaemia in rat gastric mucosa. In: British Journal of Pharmacology. 1995 ; Vol. 116, No. 4. pp. 2274-2278.
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AU - Pethő, G.

AU - Peskar, B. M.

AU - Horwell, D. C.

AU - Holzer, P.

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N2 - 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.

AB - 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.

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KW - Gall bladder contraction

KW - Gastric acid secretion

KW - Gastric mucosal blood flow

KW - Gastrin

KW - Gastrin-17

KW - Hyperaemia

KW - Vasodilatation

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