Control factors in the release of gastrin by direct electrical stimulation of the vagus

Smith, Carl C.; Kewenter, J; Connell, Alastair M.; Ardill, Joy; Hayes, R.G.J.; Buchanan, K. D.

doi:10.1007/bf01073132

Cited by 41 publications

(7 citation statements)

References 26 publications

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“…units nerve fibres within the vagus are probably not responsible for the release of 5-HT from the EC. A similar, presumably non-cholinergic (atropine-resistant) mechanism has previously been demonstrated for the vagal release of gastrin in dogs (Smith et a/. 1975).…”

Section: Discussionsupporting

confidence: 71%

A Possible Vagal Adrenergic Release of Serotonin from Enterochromaffin Cells in the Cat

Ahlman

Lundberg

Dahlström

et al. 1976

Acta Physiologica Scandinavica

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The intracellular concentrations of serotonin (5-HT) in enterochromaffin cells (EC) in the cat small intestine have been studied by a cytofluorimetric method before and after long-lasting efferent vagal nerve stimulation in the neck. Such stimulation induces a decrease of 5-HT in EC of the gut as observed previously. Pretreatment with atropine could not block this decrease, suggesting a noncholinergic mechanism. Pretreatment with a beta-blocking agent, propranolol, or bilateral removal of the superior cervical ganglia could, however, block this 5-HT decrease. Pretreatment with an alpha-blocking agent, phenoxybenzamine, caused an increase in the 5-HT content of EC both with and without nerve stimulation; the reason for this is obscure. The results indicate, that vagal nerve stimulation induces a neurogenic 5-HT release from EC in the gut, and that adrenergic fibres, originating in the superior cervical ganglia, mediate this release probably via a beta-receptor mechanism. Whether or not an alpha-receptor mechanism is also involved cannot be judged at present.

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Section: Discussionsupporting

confidence: 71%

A Possible Vagal Adrenergic Release of Serotonin from Enterochromaffin Cells in the Cat

Ahlman

Lundberg

Dahlström

et al. 1976

Acta Physiologica Scandinavica

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“…Gastrin is found in the granules of G-cells which are principally located in the gastric antrum and is released by vagal stimulation [3][4][5], Our study also showed that both pe ripheral and portal gastrin levels were in creased following electrical vagal stimulation in the control group. But in the gastrectomy group, there were no responses and the levels were significantly decreased due to the loss of G-cells.…”

Section: Discussionsupporting

confidence: 64%

Effect of Distal Gastrectomy on Gut Hormone Release following Vagal Stimulation in Dogs

Kameyama

Suzuki²,

Yasaku³

et al. 1993

Eur Surg Res

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The effect of distal gastrectomy on gut hormone release was investigated by electrical stimulation of the posterior truncal vagus in dogs. Peripheral and portal plasma gastrin release was significantly inhibited, but peripheral and portal somatostatin release was unchanged. Peripheral and portal pancreatic polypeptide (PP) release was significantly inhibited. Our results suggest that the following factors might be some of the reasons why the secretion of PP was inhibited after distal gastrectomy: (l)transection of the posterior vagal branches close to the antrum and pylorus which might go to the pancreas; (2) changes in other hormones such as gastrin; (3) elimination of the PP secretagogue from the gastric antrum.

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“…These cholinergic influences are controlled to some degree by long vago-vagal reflexes (Harper, Kidd & Scratcherd, 1959;Grossman, 1962;Debas, Konturek, Walsh & Grossman, 1974;Debas, Walsh & Grossman, 1975), and by local cholinergic reflexes which have been identified in the absence of vagal innervation (Grossman, 1961;Magee & Hu, 1975). A possible role for a local cholinergic mechanism in the control of acid secretion has been studied using atropine in animals in which the vagal innervation to the whole stomach or a fundic pouch has been severed, although it must be appreciated that atropine may also influence acid secretion by inhibiting gastrin release from the pyloric antrum; an effect which remains to be firmly established (Smith, Kewenter, Connell, Ardill, Hayes & Buchanan, 1975). In addition, gastrin has been shown to release acetylcholine from the myenteric plexus in guinea-pig ileum (Vizi, Bertaccini, Impicciatore & Knoll, 1972, 1973 and it is possible that the secretagogue action of gastrin on the stomach is partly mediated through the release of acetylcholine.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Atropine on Acid Secretion Stimulated by Acetylcholine, Histamine and Gastrin in the Isolated Whole Stomach of the Rat

Bunce¹,

Marsh²,

Parsons³

1977

British J Pharmacology

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An isolated stomach preparation from immature rats has been used to study the effect of atropine on gastric acid secretion. The acid secretory response to acetylcholine was not inhibited by atropine at a concentration of 0.3 μM. Concentrations of atropine of 1 to 3 μM produced a measurable inhibition of acid secretion, and a concentration of atropine of 10 μM caused a complete block of acid secretion which could not be surmounted by high concentrations of acetylcholine. The acid secretory response to histamine was not inhibited by concentrations of atropine of up to 1 mM. Concentrations of atropine of 1 μM and 10 μM did not inhibit gastrin‐stimulated acid secretion, although a significant inhibition of acid output was observed with atropine at concentrations of 0.1 mM and 1 mM. These findings are discussed in relation to the role of cholinergic mechanisms in the control of gastric acid secretion.

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Control factors in the release of gastrin by direct electrical stimulation of the vagus

Cited by 41 publications

References 26 publications

A Possible Vagal Adrenergic Release of Serotonin from Enterochromaffin Cells in the Cat

A Possible Vagal Adrenergic Release of Serotonin from Enterochromaffin Cells in the Cat

Effect of Distal Gastrectomy on Gut Hormone Release following Vagal Stimulation in Dogs

The Effect of Atropine on Acid Secretion Stimulated by Acetylcholine, Histamine and Gastrin in the Isolated Whole Stomach of the Rat

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