Vagal stimulation and its role in eliciting gastrin but not glucagon release from the isolated perfused dog stomach.

Lefèbvre, Pierre; Luyckx, A; Brassinne, A

doi:10.1136/gut.19.3.185

Cited by 12 publications

(2 citation statements)

References 19 publications

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“…3 In contrast, the present data show that the intra-arterial infusion of acetylcholine (or carbamylcholine) stimulated the release of glucagon from the isolated stomach. As one can see in comparing Figures 3 and 4, the glucagon-releasing effect of acetylcholine (or carbamylcholine) does not parallel the effect of these compounds on blood flow, the former being delayed while the latter occurs rapidly after initiation of the infusion.…”

Section: Cholinergic Controlcontrasting

confidence: 92%

Neurotransmitters and Glucagon Release From the Isolated, Perfused Canine Stomach

Lefèbvre

Luyckx

1980

Diabetes

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The isolated, perfused, canine stomach was used to investigate the effect of three neurotransmitters--norepinephrine, acetylcholine (or its analogue carbamylcholine), and VIP (vasoactive intestinal peptide)--on gastric glucagon release. Norepinephrine at the two concentrations tested (3.10-8 and 7.10-7 M) did not influence gastric glucagon release. In contrast, acetylcholine or carbamylcholine (5.10-6 M) as well as VIP (46-60 ng/ml) unequivocally stimulated gastric glucagon release, an effect apparently independent of the changes in blood flow. These results are in sharp contrast with the previously reported lack of effect of an electric stimulation of the vagus nerves on the release of glucagon from the dog stomach. An absence of innervation of the canine gastric A-cell would probably best explain this situation.

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Section: Cholinergic Controlcontrasting

confidence: 92%

Neurotransmitters and Glucagon Release From the Isolated, Perfused Canine Stomach

Lefèbvre

Luyckx

1980

Diabetes

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“…A number ofpeptides can be extracted from the mucosa of the GI tract that are glucagon-like in their behavior towards antisera raised against pancreatic glucagon. Lefebvre and colleagues [69] observed no glucagon release from the stomach during electrical vagal stimulation. Russell and colleagues [61] found no difference in plasma enteroglucagon levels when comparing patients with TV and SGV plus P.…”

Section: Enteroglucagonmentioning

confidence: 96%

Effect of vagotomy on gastrointestinal hormones

1979

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Different types of vagotomy have been widely used in the treatment of peptic ulcer disease. A close relationship between the vagus nerve and the release or action of gastrointestinal hormones is necessary for the optimal activation of the gastrointestinal tract. The serum concentrations of the antral hormone gastrin are elevated after all types of vagotomy. The postvagotomy hypergastrinemia is due to the change in pH in the antral lumen or the gastric motility changes, both of which may lead to a proliferation of G cells. The reduction in pancreatic secretion after vagotomy is not due to changes in intestinal hormone release, but may be caused by the interruption of a postulated enteropancreatic reflex. Postprandial GIP release and serum insulin levels are not affected by vagotomy, but basal GIP levels are increased after vagotomy. Postprandial pancreatic polypeptide release is nearly abolished by vagotomy, but seems to normalize in the later postoperative course. These findings may be important for the interpretation of pathophysiologic changes after vagotomy.

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Glucagon and Insulin Secretion

Samols¹

1983

Glucagon I

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Vagal stimulation and its role in eliciting gastrin but not glucagon release from the isolated perfused dog stomach.

Cited by 12 publications

References 19 publications

Neurotransmitters and Glucagon Release From the Isolated, Perfused Canine Stomach

Neurotransmitters and Glucagon Release From the Isolated, Perfused Canine Stomach

Effect of vagotomy on gastrointestinal hormones

Glucagon and Insulin Secretion

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