Effect of secretin on gastric acid and pepsin secretion in response to various stimuli

Nakajima, Sumio; Nakamura, Michio; Df, Magee

doi:10.1152/ajplegacy.1969.216.1.87

Cited by 49 publications

(9 citation statements)

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“…In the dog, a striking feature of the pepsin response is inhibition by higher doses of histamine. This is shown in both innervated (2, 8, 11, 12, 16, 19-22, 27, 33) and denervated mucosa (2,11,21,27,29,32,33). Histamine suppresses the pepsin response to vagal stimulation by insulin (17) "on-active' and Stimulated Secretion 947 of pepsin continues, so that the chief cells contain progressively more granules during prolonged infusion of histamine (6,18).…”

Section: Discussionmentioning

confidence: 97%

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‘Non-Active’ Pepsin Secretion Compared with Stimulated Secretion by Bethanechol, Histamine, Pentagastrin, and 2-Deoxy-D-Glucose

Guldvog¹,

Gedde-Dahl²,

Berstad³

1980

Scandinavian Journal of Gastroenterology

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The present studies were performed on a double-pouch dog with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl, 0.15 M NaCl, and 0.03 M phosphate buffer, and well-known stimulators of gastric secretion such as histamine, pentagastrin, bethanechol, and 2-deoxy-D-glucose (2-DG) were tested as pepsigogues. Cholinergic stimulation by 2-DG and bethanechol (Urecholine) was clearly the most potent stimulus of pepsin secretion. 2-DG elicited secretion only from innervated mucosa, whereas the responses to bethanechol were similar in the two pouches. Histamine and pentagastrin were weak stimulators, but both provoked active and sustained secretion of pepsin when given in small doses. Higher doses of histamine strongly inhibited pepsin output. The effects of histamine were independent of vagal innervation. By contrast, the active stimulation by pentagastrin only took place in innervated mucosa. The highest outputs were seen in the lowest doses, but also very high doses of pentagastrin elicited active pepsin secretion in the AP. Medium doses of pentagastrin brought the secretion down the the 'non-active' level. The chief cells in the denervated mucosa were quite insensible to pentagastrin, and the pepsin output in the HP equalled the non-active' response at all dose levels.

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Section: Discussionmentioning

confidence: 97%

“…Different means of vagal activation are unique for the stimulation of pepsin secretion (4,21,22,27,31,32,35,36). The present responses to 2-DG and bethanechol confirm this.…”

Section: Discussionmentioning

confidence: 99%

‘Non-Active’ Pepsin Secretion Compared with Stimulated Secretion by Bethanechol, Histamine, Pentagastrin, and 2-Deoxy-D-Glucose

Guldvog¹,

Gedde-Dahl²,

Berstad³

1980

Scandinavian Journal of Gastroenterology

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“…However, this occurs at a period in the digestive process when secretin is physiologically acting to reduce gastric motility and acid secretion. As its action on the latter two functions is to return them to their basal level (9)(10)(11)(12)(13)(14), the action of secretin on sphincter competence seems well adapted to returning this function back to resting competent levels. It is only with pharmacological doses of secretin that sphincter pressure can be brought below normal resting levels.…”

Section: Discussionmentioning

confidence: 99%

“…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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“…Secretin stimulates secretion o f pepsin in man (1,5), dog (14,15,17) and cat (4,5). Both natural and synthetic secretin act on gastric secretion (19).…”

mentioning

confidence: 99%

Effect of Secretin on the Secretion of Acid and Pepsin by the Totally Isolated Canine Stomach

Kowalewski¹,

Kolodej²

1974

Pharmacology

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Totally isolated whole canine stomachs, perfused ex vivo with homologous blood, were used for study of the action of secretin on gastric secretion of acid and pepsin. During 8 h of perfusion, stomachs were stimulated by constant infusion of pentagastrin, 32 μg/h, into gastric arteries of isolated organs. When base line secretion was established (3.5 h), secretin, 60 U/h, was also infused for 90 min into the gastric artery. Secretin injection was then interrupted, but pentagastrin infusion continued until the termination of the experiment. Secretin reduced the volume of secretion and the concentration and output of HC1. Secretin also increased the concentration and output of pepsin. Dissociated effect of secretin on gastric acid and pepsin secretion by totally isolated in vivo perfused canine stomachs resembles the action of secretin on gastric secretion, reported by others, in various in vivo experiments.

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Effect of secretin on gastric acid and pepsin secretion in response to various stimuli

Cited by 49 publications

References 0 publications

‘Non-Active’ Pepsin Secretion Compared with Stimulated Secretion by Bethanechol, Histamine, Pentagastrin, and 2-Deoxy-D-Glucose

‘Non-Active’ Pepsin Secretion Compared with Stimulated Secretion by Bethanechol, Histamine, Pentagastrin, and 2-Deoxy-D-Glucose

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

Effect of Secretin on the Secretion of Acid and Pepsin by the Totally Isolated Canine Stomach

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