Physiologic mechanisms inhibiting gastric secretion of acid

Andersson, Sven

doi:10.1016/0002-9610(69)90072-5

Cited by 13 publications

(11 citation statements)

References 42 publications

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“…However our findings that intraduodenal fat is the least potent stimulus of plasma GIP release into the peripheral circulation is in keeping with current understanding of the physiological function of circulating GIP. It has long been known that intraduodenal infusion of solutions of fat but not protein or isotonic glucose is a potent inhibitor of gastric acid secretion in dogs and man (Anderson, 1967). This inhibitory response is thought to be mediated by release of one or more circulating hormones, which have been termed 'enterogastrones'.…”

Section: Discussionmentioning

confidence: 99%

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Lucey

Fairclough

Wass

et al. 1984

Clinical Endocrinology

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We have studied the effect of direct infusion of nutrients into the duodenum of normal subjects on circulating plasma somatostatin, insulin, gastrin and gastric inhibitory polypeptide (GIP) levels. Six normal subjects were given on four separate occasions 150 ml of isotonic solutions containing 100 calories of carbohydrate, protein, or fat, and a control solution of saline, by infusion into the second part of the duodenum. Plasma somatostatin rose slightly after carbohydrate, mean basal 30 +/- 3 pg/ml, peak 46 +/- 16 pg/ml at 15 min; and more markedly after protein, peak 57 +/- 9 pg/ml at 30 min. However, fat was the most potent intraduodenal stimulus to plasma somatostatin release into circulation, peak 101 +/- 11 pg/ml at 30 min. The plasma insulin rise was greatest after carbohydrate, peak 68 +/- 10 i.u., but there was a significant rise after protein also, peak 34 +/- 6 i.u. Plasma gastrin rose significantly after protein only, peak 70 +/- 22 pg/ml. Plasma GIP rose markedly after carbohydrate, basal 506 +/- 50 pg/ml, peak 1480 +/- 120 pg/ml. Protein was also a potent stimulus of circulating plasma GIP release, peak 1200 +/- 190 pg/ml, while fat was the least potent, peak 730 +/- 190 pg/ml. Thus, calorie for calorie, fat is the most potent intraduodenal nutrient stimulus of circulating somatostatin. We postulate therefore that somatostatin may be an enterogastrone--a circulating hormone released by intraduodenal fat which inhibits gastric acid secretion. Fat is the least potent intraduodenal nutrient stimulus of circulating GIP release. This is evidence against the hypothesis that circulating GIP acts as an enterogastrone.

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Section: Discussionmentioning

confidence: 99%

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Lucey

Fairclough

Wass

et al. 1984

Clinical Endocrinology

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“…Clearly more juice was lost from the control stomachs than from those receiving FPL 52694. Acidification of the duodenum is well known to cause inhibition of pentagastrin-stimulated acid secretion but results during histamine stimulation are more variable (Andersson, 1967). Thus, it seems likely that acid is lost from the stomach in control experiments leading to a degree of secretory inhibition which was greater with pentagastrin than with his-tamine.…”

Section: Intragastric Control Experimentsmentioning

confidence: 99%

Inhibition of gastric acid secretion in the conscious dog by the mast‐cell stabilizing agent, FPL 52694

Canfield

Curwain

1983

British J Pharmacology

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1 The effects of the mast-cell stabilizing agent, FPL 52694, on gastric acid secretion in conscious dogs with gastric fistulae have been studied. 2 FPL 52694 (5 or 10mg kgl h-) given intravenously during a plateau response to pentagastrin stimulation (21ggkg-I h-1) caused a maximum inhibition of acid output of about 50% but had no significant effect on volume output so that the [H+] in the juice was markedly reduced. The ratio of mucosal blood flow/acid output (Ra) was increased in the presence of FPL 52694. There was no maintained reduction of [H+] when inhibition was due to cimetidine (41mol kg-', i.v.).3 Instillation of FPL 52694 (4.35 mg ml-l) directly into the stomach via the fistula for 30 min also resulted in an inhibition of acid output and reduction of [HI] during both pentagastrin-(2 pg kg-l h-1) and histamine-stimulated (301 g kg-l h-1) secretion. Inhibition of pentagastrinstimulated acid output by intragastric administration of FPL52694 was much greater than the maximum effect seen following intravenous infusion. 4 The results are discussed in relation to the possible mode of action of FPL 52694. It is concluded that FPL 52694 is active orally and has a novel action on acid secretion which may include stimulation of gastric bicarbonate secretion.

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“…It is now generally accepted that in the intact stomach, the effectiveness of secretary stimulation is greatly decreased when gastric content is acidified. This acid-induced inhibition of gastric secretion has been attributed to the antral and duodenal feed-back inhibitory mechanisms (Andersson, 1967) but no attempt has been made to determine the possible autoregulation of gastric secretion arising from the oxyntic gland area itself.…”

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confidence: 99%

Characteristics of gastric inhibition by acidification of oxyntic gland area.

Konturek¹,

Obtulowicz²,

Tasler³

1975

The Journal of Physiology

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SUMMARY1. Gastric acid responses to the test meals were measured in the Heidenhain pouch, gastric and pancreatic fistula dogs, using the intragastric titration method, and monitoring the rate at which a solution of 1 0 N-NaOH had to be added to maintain the pH of the gastric content constant at preselected values ranging from 5 0 to 1.0. In this way the pH profile of the gastric acid and pepsin responses to a liver extract meal kept in the Heidenhain pouch or gastric fistula as well as to exogenous stimuli such as histamine, pentagastrin or Urecholine, could be determined.2. A liver extract meal adjusted to pH 5 0 produced a potent and pressure-related stimulation of acid secretion from the Heidenhain pouch without any change in secretion from the main stomach and pancreas or in the serum concentration of immuno-assayable gastrin.3. Graded decrease of the liver extract meal pH to below 5.0 resulted in the pH-dependent inhibition of gastric acid output, which at pH 1.0 was only about 30 % of the value attained at pH 5 0. Acid secretion from the Heidenhain pouch induced by exogenous stimuli such as histamine, pentagastrin or Urecholine also showed gradual decrease when the pH of the pouch content was decreased in sequential order from 5 0 to 1X0. This pH-dependent inhibition was accompanied by an increase in pepsin secretion.4. The pH-dependent inhibition of the Heidenhain pouch response to the liver extract meal was not altered by topical application of a local anaesthetic and atropine or by the intravenous infusion of large doses of atropine, secretin or metiamide, which were shown to cause a marked inhibition of the main stomach response to the liver meal.5. The results indicate that there is a local and gastrin-independent inhibition mechanism of gastric acid secretion activated by an acidified meal making contact with the oxyntic gland area. STANISLA W J. KONTUREK AND OTHERS

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Physiologic mechanisms inhibiting gastric secretion of acid

Cited by 13 publications

References 42 publications

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Inhibition of gastric acid secretion in the conscious dog by the mast‐cell stabilizing agent, FPL 52694

Characteristics of gastric inhibition by acidification of oxyntic gland area.

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