Influences of duodenal acidification on acid and pepsin secretion of the stomach in dogs

Nakajima, Sumio; Df, Magee

doi:10.1152/ajplegacy.1970.218.2.545

Cited by 30 publications

(8 citation statements)

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“…This observation was consistent with the antagonism of gastrin I for secretin and cholecystokinin on the pyloric muscle since duodenal acidification releases both hormones (4,5). The relevance of these observations to the function of the pylorus must be interpreted cautiously.…”

Section: Discussionsupporting

confidence: 81%

“…The mechanism by which the human pylorus contracts in response to the intraduodenal instillation of amino acids, olive oil, and HC1 is not known. It has been presumed to be hormonal because the substances which were instilled into the duodenum are known to release both secretin and cholecystokinin (4)(5)(6)(7)(8)(9)(10)(11). In addition, a precedent for hormonal regulation of other gastrointestinal sphincters has been established (12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

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The Hormonal Regulation of Pyloric Sphincter Function

Fisher¹,

Lipshutz²,

Cohen³

1973

J. Clin. Invest.

120

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A B S T R A C T The purpose of this study was to evaluate the hormonal control of pyloric sphincter function. Studies were performed on both pyloric circular muscle, in vitro, and the human pylorus, in vivo. Full dose-response curves to gastrin I, cholecystokinin, and secretin were constructed for the pyloric muscle of the opossum studied at its length of optimal tension development, Lo. Both cholecystokinin and secretin were potent agonists on the muscle but gastrin I gave no increase in muscle tension. The combination of cholecystokinin and secretin was additive at submaximal concentrations but potentiation of the maximal responses was not observed. Gastrin I produced a surmountable, competitive-like antagonism to the effect of cholecystokinin on the pyloric muscle. The octapeptide of cholecystokinin was a more potent agonist than the whole molecule of cholecystokinin on the pyloric muscle. In man, the pyloric pressure rose significantly during intravenous infusion of either cholecystokinin or secretin. The combination of maximal doses of both hormones did not show signficant potentiation. Gastrin I did not significantly increase pyloric pressure but did antagonize the pyloric response to duodenal acidification. These studies suggest that: (a) Both secretin and cholecystokinin augment pyloric sphincter pressure while gastrin I is an antagonist inhibiting their effects. (b) The hormonal responses of pyloric sphincter circular muscle, in vitro, can be correlated with human sphincter function, in vivo.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

The Hormonal Regulation of Pyloric Sphincter Function

Fisher¹,

Lipshutz²,

Cohen³

1973

J. Clin. Invest.

120

View full text Add to dashboard Cite

show abstract

“…When the pH fell below 215 the secretion of acid and pepsin in response to food and insulin was inhibited. Nakajima & Magee (1970) confirmed these results in Heidenhain pouch dogs. The observation that acid in the duodenum releases secretin when the pH is less than 5 (Meyer & Grossman, 1971) suggested that the intestinal hormone responsible for the physiological control of peptic secretion might indeed be secretin.…”

Section: Discussionsupporting

confidence: 75%

A comparison of the pepsin stimulating effects of secretin preparations.

Braganza¹,

Howat²,

Kay³

1976

The Journal of Physiology

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The slopes of the log dose-response lines were significantly different for these two products indicating that their modcs of action in stimulating pepsin may not be identical.3. The outputs of pepsin following GIH and synthetic secretin were similar. Both these secreting stimulated the secretion of pepsin when infused in doses which stimulated the pancreas supramaximally. The less pure product Boots secretin evoked significantly higher peptic responses at doses submaximal for pancreatic stimulation, suggesting that a substance other than secretin exists in Boots preparations which contributes significantly to the overall output of pepsin in response to this product. The peptic response which was accompanied by a slight increase in acid output, but without any increase in pancreatic lipolytic activity, was not inhibited by atropine. This substance which is not present in highly purified GIH secretin does not appear to be cholic acid, gastrin, pancreozymin, glucagon or insulin. 3PHY 258 64 J. M. BRAGANZA, H. T. HOWAT AND G. H. KAY 4. The possibility that a vasodilator substance is present in Boots secretin which by expanding the splanchnic bed increases the concentration of secretin at target sites in the stomach and pancreas seems unlikely, as the flow of pancreatic juice does not increase proportionately with the vast increase in pepsin. A vasodilator substance which specifically affects the gastric vasculature remains a theoretical but unlikely explanation for our observation.

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“…Recently, it has been shown that the gastrointestinal hormone, gastrin, has a physiological role in the control of sphincter strength (5,6). Since a well-known relationship exists between gastrin and secretin in the hormonal control of gastric acid secretion (7)(8)(9)(10)(11)(12) and gastric motor function (13)(14), it seemed possible that these hormones also interact to regulate lower esophageal sphincter competence. This study is designed to quantitatively assess the interaction of endogenous and exogenous gastrin and secretin in the regulation of lower esophageal sphincter competence in man.…”

Section: Introductionmentioning

confidence: 99%

Hormonal regulation of human lower esophageal sphincter competence: interaction of gastrin and secretin

Cohen¹,

Lipshutz²

1971

J. Clin. Invest.

205

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A BSTRACT The interaction of gastrin and secretin, in the regulation of human lower esophageal sphincter competence, was studied in 54 normal subjects. A doseresponse curve, for the lower esophageal sphincter, was constructed from the rapid intravenous injections of synthetic gastrin I (amino acid sequence 2-17). This curve was sigmoid shaped and showed a peak response that was 460.0 ±24.0% (mean ±2 SE) of the initial sphincter pressure, at a dose of 0.7 /g/kg of gastrin I. Secretin, either endogenously released by duodenal acidification, or exogenously administered as a single intravenous injection, markedly reduced the peak response of the sphincter to gastrin I. To ascertain the character of this inhibition, a gastrin I dose-response curve was obtained during a continuous intravenous secretin infusion. This curve showed a parallel shift to the right, with the maximal sphincter response to gastrin I still attainable at higher doses. A sphincter, endogenously stimulated by gastrin, showed a dose-related reduction in pressure with rapid intravenous injections of secretin. At the level of resting sphincter pressure, response to secretin diminished, and larger doses were required for comparable reduction in pressure. These studies indicate: (a) Secretin interacts with gastrin in the physiological regulation of human lower esophageal sphincter competence; (b) Secretin is a sensitive inhibitor to gastrin stimulation of the lower esophageal sphincter; (c) This inhibitory effect of secretin is competitive in character.

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Influences of duodenal acidification on acid and pepsin secretion of the stomach in dogs

Cited by 30 publications

References 0 publications

The Hormonal Regulation of Pyloric Sphincter Function

The Hormonal Regulation of Pyloric Sphincter Function

A comparison of the pepsin stimulating effects of secretin preparations.

Hormonal regulation of human lower esophageal sphincter competence: interaction of gastrin and secretin

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