Displacement by Metiamide of the Dose‐response Curves to Pentagastrin and Methacholine in the Conscious Rat

Lundell, Lars

doi:10.1111/j.1476-5381.1975.tb07598.x

Cited by 11 publications

(4 citation statements)

References 11 publications

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“…The reduction of the maximal response to gastrin in the presence of metiamide (Figure 4) is compatible with a non-competitive type of inhibition, and is similar to results obtained in vivo using pentagastrin in the Heidenhain pouch rat (Lundell, 1975), and by Black (1973) using the Heidenhain pouch dog. However metiamide has been shown to act like a competitive antagonist at H2-receptors (Parsons, 1973;Bunce & Parsons, 1976), and this situation led Black (1973) to postulate that canine gastric mucosa possesses two types of gastrin receptor.…”

Section: Discussionsupporting

confidence: 86%

The Effect of Metiamide on Acid Secretion Stimulated by Gastrin, Acetylcholine and Dibutyryl Cyclic Adenosine 3′, 5′‐monophosphate in the Isolated Whole Stomach of the Rat

Bunce¹,

Parsons²,

Rollings³

1976

British J Pharmacology

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I An isolated stomach preparation from immature rats is described. The lumen of the stomach was perfused and the hydrogen ion activity of the perfusate recorded continuously. 2 The preparation gave dose-dependent responses to gastrin, acetylcholine and dibutyryl cyclic adenosine 3',5'-monophosphate and these responses were readily reversed on washing out the agonist. 3 The acid secretory response to gastrin was inhibited by metiamide at concentrations of 10-M and 3 x 1O-5M. 4 The acid secretory responses to acetylcholine and dibutyryl cyclic adenosine 3',5'-monophosphate were not inhibited by concentrations of metiamide up to 103 M. 5 These findings are discussed in relation to the role of histamine in the control of gastric acid secretion.

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Section: Discussionsupporting

confidence: 86%

The Effect of Metiamide on Acid Secretion Stimulated by Gastrin, Acetylcholine and Dibutyryl Cyclic Adenosine 3′, 5′‐monophosphate in the Isolated Whole Stomach of the Rat

Bunce¹,

Parsons²,

Rollings³

1976

British J Pharmacology

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“…In addressing the question of whether gastric acid secretion modifies chemosensory afferent inputs from the gastric lumen, we used cimetidine and omeprazole at doses known to effectively suppress basal and stimulated gastric acid secretion in the rat: cimetidine at the dose of 40 mol/kg (5), omeprazole at the dose of 20 mol/kg (24), and pentagastrin at a dose (195 mol/kg) that maximally increases gastric acid secretion in the rat (26). Because cimetidine failed to alter the NTS response to intragastric NH 4 OH, it can be ruled out that NH 4 OH led to stimulation of vagal afferents because it facilitated the backdiffusion of luminal acid through the NH 4 OH-compromised gastric mucosa or because it increased gastrin and gastric acid secretion (30).…”

Section: Discussionmentioning

confidence: 99%

Stomach-brain communication by vagal afferents in response to luminal acid backdiffusion, gastrin, and gastric acid secretion

Danzer¹,

Jocič²,

Samberger³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Vagal afferents play a role in gut-brain signaling of physiological and pathological stimuli. Here, we investigated how backdiffusion of luminal HCl or NH(4)OH and pentagastrin-stimulated acid secretion interact in the communication between rat stomach and brain stem. Rats were pretreated intraperitoneally with vehicle or appropriate doses of cimetidine, omeprazole, pentagastrin, dexloxiglumide (CCK(1) receptor antagonist), and itriglumide (CCK(2) receptor antagonist) before intragastric administration of saline or backdiffusing concentrations of HCl or NH(4)OH. Two hours later, neuronal activation in the nucleus of the solitary tract (NTS) and area postrema was visualized by c-Fos immunohistochemistry. Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH(4)OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTS, which was not related to gender, gastric mucosal injury, or gastropyloric motor alterations. The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide. Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide. We conclude that vagal afferents transmit physiological stimuli (gastrin) and pathological events (backdiffusion of luminal HCl or NH(4)OH) from the stomach to the brain stem. These communication modalities interact because, firstly, acid secretion enhances afferent signaling of gastric acid backdiffusion and, secondly, gastrin activates NTS neurons through stimulation of CCK(1) receptors on vagal afferents and of CCK(2) receptors on area postrema neurons projecting to the NTS.

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“…In vivo studies using histamine H2-receptor antagonists have shown that these compounds inhibit acid secretion in response to histamine, gastrin (or pentagastrin) and cholinergic stimulation (Parsons, 1975). However the acid response to cholinergic stimulation is more resistant to inhibition by H2-receptor antagonists than the response to pentagastrin (Black, 1973;Lundell, 1975a).…”

Section: Introductionmentioning

confidence: 99%

Inhibition by metiamide of secretagogue‐induced gastric acid secretion in the conscious Heidenhain pouch rat.

Bunce¹,

Parsons²

1978

The Journal of Physiology

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i.v. did produce a significant inhibition. In contrast with histamine and pentagastrin, metiamide inhibited bethanechol-stimulated secretion only by reducing acid concentration; there was no significant decrease in the gastric secretary volume. 5. It is concluded that these results are consistent with the view that histamine and pentagastrin share a common pathway in stimulating gastric acid secretion in the rat. The role of histamine in the control of bethanechol-stimulated acid secretion remains unclear.

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Displacement by Metiamide of the Dose‐response Curves to Pentagastrin and Methacholine in the Conscious Rat

Cited by 11 publications

References 11 publications

The Effect of Metiamide on Acid Secretion Stimulated by Gastrin, Acetylcholine and Dibutyryl Cyclic Adenosine 3′, 5′‐monophosphate in the Isolated Whole Stomach of the Rat

The Effect of Metiamide on Acid Secretion Stimulated by Gastrin, Acetylcholine and Dibutyryl Cyclic Adenosine 3′, 5′‐monophosphate in the Isolated Whole Stomach of the Rat

Stomach-brain communication by vagal afferents in response to luminal acid backdiffusion, gastrin, and gastric acid secretion

Inhibition by metiamide of secretagogue‐induced gastric acid secretion in the conscious Heidenhain pouch rat.

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