Adenylate cyclase and H+ production of isolated rat parietal cells in response to glucagon and histamine

Schepp, Wolfgang; Ruoff, H. J.

doi:10.1016/0014-2999(84)90103-1

Cited by 28 publications

(12 citation statements)

References 36 publications

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“…They are about 100 times more potent than L-365,260 (Ding & Hikanson 1996), the compound first classified as a selective cholecystokinin-B/gastrin receptor antagonist in the late 1980s (Lotti & Chang 1989). Gastrin is a powerful stimulus for gastric acid secretion but whether cholecystokinin-B/gastrin receptors exist on the parietal cells has been debated (Dial et al 1981;Schepp & Ruoff 1984;Cabero et al 1991). The ECL cells are known to be rich in cholecystokinin-B/gastrin receptors (Chiba et al 1991;Nakata et al 1992;Asahara et al 1994;Song et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Three Novel Cholecystokinin‐B/Gastrin Receptor Antagonists: A Study of their Effects on Rat Stomach Enterochromaffin‐Like Cell Activity

Ding

Lindström

Håkanson

1997

Pharmacology & Toxicology

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Gastrin stimulates rat stomach enterochromaffin-like (ECL) cells via activation of cholecystokinin-Blgastrin receptors. The stimulation is manifested in the activation of the histamine-forming enzyme histidine decarboxylase and in the secretion of histamine and pancreastatin, a chromogranin A-derived peptide. We have examined the short-term effects of three novel cholecystokinin-B/gastrin receptor antagonists (YF476, JB93182 and AG041R) on the ECL cells in intact fasted rats. The drugs and/or gastrin were infused intravenously for 3 hr and the oxyntic mucosal histidine decarboxylase activity and the serum pancreastatin concentration were measured. We also studied the effects of the three drugs on gastric emptying in mice, a cholecystokinin-A receptor-nediated response. YF476, JB93182 and AG041R antagonized the gastrin-evoked histidine decarboxylase activation in a dose-dependent manner. YF476, JB93182 and AGO41 R induced maximal inhibition at 0.03, 0.1 and 0.1 pmol kg-' hr-I, respectively; the corresponding IDso values were 0.002, 0.008, and 0.01 pmol kg-' hr-'. YF476 was selected for further analysis. It produced a rightward shift of the gastrin doseresponse curve, consistent with competitive inhibition. Moreover, it antagonized the omeprazole-evoked histidine decarboxylase activation and the gastrin-and omeprazole-induced rise in the circulating pancreastatin concentration. None of the three drugs tested inhibited gastric emptying or prevented the cholecystokinin-8s-induced inhibition of gastric emptying at the doses tested. The results show that YF476, JB93182 and AG041R are potent and selective cholecystokinin-B/ gastrin receptor antagonists, and that YF476 is 4-5 times more potent than JB93182 and AG041R.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Three Novel Cholecystokinin‐B/Gastrin Receptor Antagonists: A Study of their Effects on Rat Stomach Enterochromaffin‐Like Cell Activity

Ding

Lindström

Håkanson

1997

Pharmacology & Toxicology

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“…The en zymes used in most cell isolation procedures are pronase and collagenase. In several pub lished reports using parietal cells from pronase-digested rat stomachs, it has been shown that vaso-active intestinal polypep tide, secretin, cholecystokinin, somatostatin, glucagon and prostaglandins can directly af fect the parietal cells [22][23][24], In our study, the functional integrity of the parietal cells was demonstrated by the results of histamine stimulation and by electron microscopy. These findings suggest that the receptors re main unaffected by the isolation procedure.…”

Section: Discussionmentioning

confidence: 85%

“…(2) Could endogenous prostaglandin formed during the isolation procedure affect the re sponsiveness of the parietal cell to the secretagogue action of, e.g., GRP? It has been reported that prostaglandin Et inhibits hista mine-stimulated gastric acid secretion in rat and dog parietal cells [22][23][24], We tested this by adding the cyclo-oxygenase inhibitor indomethacin (10 mg/1) to the incubation mix ture but found no effect on the responsive ness of parietal cells to GRP or histamine (results not shown). This is in agreement with previous studies [21],…”

Section: Discussionmentioning

confidence: 99%

The Gastric Acid Secretagogue Gastrin-Releasing Peptide and the Inhibitor Oxyntomodulin Do Not Exert Their Effect Directly on the Parietal Cell in the Rat

et al. 1988

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Previous studies suggested that gastrin-releasing peptide (a neuropeptide found in rat oxyntic mucosa) and oxyntomodulin (a glucagon-containing peptide of mammalian gut) could directly affect the acid secretion of the parietal cells. We therefore studied their effect on gastric acid production in vitro by measuring [¹⁴C]-aminopyrine accumulation, a reliable index of H⁺ generation, in isolated rat parietal cells. However, neither gastrin-releasing peptide nor oxyntomodulin influenced basal acid secretion or histamine-stimulated gastric acid secretion. Electron-microscopic studies of unstimulated and histamine-stimulated parietal cells confirmed that the cells retained the normal morphology of intracellular organelles and that the cells responded to physiological stimulation by marked expansion of the intracellular canaliculi.

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“…However, in rat (Schepp & Ruoff, 1984) and human (Miederer et al 1986) parietal cells the effects of glucagon and histamine on adenylate cyclase activity were additive. Glucagon did not increase aminopyrine accumulation in rat parietal cells (Schepp & Ruoff, 1984 (Kromer, Schroder & Netz, 1984;Schepp, Schneider, Schusdziarra & Classen, 1986). The effects of these opioid peptides were blocked by (-)naloxone.…”

Section: Glucagon and Related Peptides?mentioning

confidence: 99%

Intracellular Signalling and Regulation of Gastric Acid Secretion

Hanson

Hatt

1989

Exp Physiol

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Adenylate cyclase and H+ production of isolated rat parietal cells in response to glucagon and histamine

Cited by 28 publications

References 36 publications

Evaluation of Three Novel Cholecystokinin‐B/Gastrin Receptor Antagonists: A Study of their Effects on Rat Stomach Enterochromaffin‐Like Cell Activity

Evaluation of Three Novel Cholecystokinin‐B/Gastrin Receptor Antagonists: A Study of their Effects on Rat Stomach Enterochromaffin‐Like Cell Activity

The Gastric Acid Secretagogue Gastrin-Releasing Peptide and the Inhibitor Oxyntomodulin Do Not Exert Their Effect Directly on the Parietal Cell in the Rat

Intracellular Signalling and Regulation of Gastric Acid Secretion

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