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Inhibition of Gastric Acid Secretion

Stanisław J. Konturek

10.1002/cphy.cp060309

Source: Supplement 18: Handbook of Physiology, The Gastrointestinal System, Salivary, Gastric, Pancreatic, and Hepatobiliary Secretion

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Cephalic Inhibition of Gastric Secretion
1.1 Cephalic Phase
1.2 Inhibition of Cephalic Phase
2 Inhibition Arising from Stomach
2.1 Gastric Phase
2.2 Inhibition Arising from Oxyntic Mucosa
2.3 Inhibition Arising from Antral Mucosa
2.4 Pharmacological Inhibition of Gastric Phase
3 Intestinal Inhibition of Gastric Secretion
3.1 Intestinal Phase
3.2 Intestinal Inhibition by Acid
3.3 Intestinal Inhibition by Fat
4 Gastric Inhibition by Urogastrone and Epidermal Growth Factor
5 Gastric Inhibition by Neuropeptides
5.1 Gastric Inhibitory Effects of Neuropeptides Administered Intracerebrally
5.2 Gastric Inhibitory Effects of Neuropeptides Administered Intravenously
6 Sympathetic Nervous System and Gastric Inhibition
Figure 1. Figure 1.

A: gastric fistula acid output; B: plasma gastrin; C: somatostatin‐like immunoreactivity increments over basal levels in response to insulin hypoglycemia before and >3 days after truncal vagotomy in dogs.

From Hollinshead et al. 70. Copyright 1985 by The American Gastroenterological Association
Figure 2. Figure 2.

Mean acid output from gastric fistula and plasma gastrin and somatostatin‐like immunoreactivity, SLI, before and after sham feeding, SF, 10 min) in dogs without and with intravenous injection of atropine, A, at dose of 20 or 100 μg/kg.

From De Graef and Woussen‐Colle 30
Figure 3. Figure 3.

Mean ± SE acid response to modified sham feeding, MSF, and pentagastrin infusion 2 μg·kg‐1·h‐1) in duodenal ulcer patients (n = 6‐8) without and with administration of pirenzepine, cimetidine or ranitidine, 16,16‐dimethyl prostaglandin E2 16,16 DMPGE2), or omeprazole. Single asterisk, P < 0.05; double asterisk, P <0.01.

From Konturek 93
Figure 4. Figure 4.

Mean acid outputs from Heidenhain pouch, HP, in response to graded doses of intravenous pentagastrin, histamine, or 15% liver extract meal, LE, before, pre‐op, and after, post‐op, excision of fundic mucosa.

From Soon‐Shiong and Debas 197. Copyright 1980 by The American Gastroenterological Association
Figure 5. Figure 5.

Responses to 300‐ml liquid meal of 15% liver extract in control stage, C, after truncal vagotomy, AV, and after proximal gastric vagotomy, PGV. A: plasma gastrin increment over basal aftermeal (n = 6 dogs); B: first 4‐h gastric fistula acid output in response to meal (n = 6 dogs); C: Heidenhain pouch acid output in response to meal in three stages (n = 3 dogs).

From Debas et al. 27
Figure 6. Figure 6.

Effects of distension of vagally innervated antral pouch with 100 mM NaHCO3 or 100 mM HCl on acid output from vagally innervated gastric fistula and on increments in serum gastrin concentrations. Acidification of antral pouch abolished gastrin release but only moderately reduced acid output, indicating that pylorooxyntic reflex was operating. Vagal denervation of antral pouch abolished the effect.

From Debas et al. 28
Figure 7. Figure 7.

Mean serum gastrin level (top) and gastric acid secretion (bottom) in response to amino acid meal of varying pH in duodenal ulcer, DU, (n = 9) and normal subjects (n = 12). Single asterisk, significant increase above basal levels; double asterisk, significant difference between duodenal ulcer and normal subjects; triple asterisk, significantly less than peak.

From Thompson and Swierczek 217
Figure 8. Figure 8.

Effect of acidification of duodenal bulb before and after separation from pylorus or of exogenous secretin infused in small (.2 U·kg‐1·h‐1) and large 1.6 U·kg‐1·h‐1) doses on gastric acid secretion from gastric fistula and on plasma secretin levels.

Adapted from Konturek and Johnson 112
Figure 9. Figure 9.

Effects of immunoneutralization of circulating secretin on serum gastrin and gastric acid responses to 5% liver extract, LE, meals in stomach adjusted to pHs varying from 7.0 to 2.0 or to 5% liver extract meal of pH 7.0 combined with intravenous infusion of graded doses of secretin (.03 ‐ 2.0 U·kg‐1·h‐1). Mean ± SE of 10 tests on 5 dogs with gastric and pancreatic fistulas. Secretin antiserum almost completely removed circulating secretin both in tests with meals of varying pH and exogenous secretin. Single asterisk, signifcantly different from control.

From Konturek et al. 105
Figure 10. Figure 10.

Effects of intravenous infusion of exogenous gastric inhibiting peptide, GIP, 1.0 μg·kg‐1·h‐1) or fat administered intraduodenally or intravenously on gastric acid secretion from Heidenhain pouch and gastric fistula stimulated by liver extract meal of pH 5.5 in main stomach (left) and serum GIP and gastrin levels (right) in dogs. Mean ± SE of 6 tests or 6 dogs. Single asterisk, significantly different from control.

From Konturek et al. 113
Figure 11. Figure 11.

Gastric acid and plasma neurotensin concentration during infusion of pentagastrin 150 ng·kg‐1·h‐1) and neurotensin (500 ng·kg‐1·h‐1) in 7 duodenal ulcer patients before (A) and after (B) parietal cell vagotomy.

From Olsen et al. 156
Figure 12. Figure 12.

Effect of epidermal growth factor (EGF) 1.0 μg·kg‐1·h‐1) on acid secretion from gastric fistula and Heidenhain pouches stimulated by pentagastrin 2.0 μg·kg‐1·h‐1), histamine 40 μg·kg‐1·h‐1), or urecholine 100 μg·kg‐1·h‐1). Single asterisk, significantly different from control.

From Konturek at al. 102
Figure 13. Figure 13.

Inhibitory effects of gastrin‐releasing peptide (GRP) on gastric acid output in pylorus‐ligated rats stimulated by intracisternal thyrotropin‐releasing hormone (TRH), 2‐deoxy‐d‐glucose 2‐DG), or histamine (HIS) without and with intracisternal administration of GRP.

From Taché et al. 205. Copyright 1981 by The American Gastroenterological Association
Figure 14. Figure 14.

Model for regulation of gastrin and somatostatin release in antrum by cholinergic and noncholinergic (bombesinergic) intramural neurons. Somatostatin (SS) cell is shown structurally and functionally coupled to gastrin cell. Sensory bipolar neuron links the regulatory cholinergic (ACh) and bombesinergic (BOM) neurons to luminal stimulus. Luminal stimulus could act directly on gastrin and somatostatin cells.

From Saffouri et al. 176. Copyright 1984 by The American Gastroenterological Association


Figure 1.

A: gastric fistula acid output; B: plasma gastrin; C: somatostatin‐like immunoreactivity increments over basal levels in response to insulin hypoglycemia before and >3 days after truncal vagotomy in dogs.

From Hollinshead et al. 70. Copyright 1985 by The American Gastroenterological Association


Figure 2.

Mean acid output from gastric fistula and plasma gastrin and somatostatin‐like immunoreactivity, SLI, before and after sham feeding, SF, 10 min) in dogs without and with intravenous injection of atropine, A, at dose of 20 or 100 μg/kg.

From De Graef and Woussen‐Colle 30


Figure 3.

Mean ± SE acid response to modified sham feeding, MSF, and pentagastrin infusion 2 μg·kg‐1·h‐1) in duodenal ulcer patients (n = 6‐8) without and with administration of pirenzepine, cimetidine or ranitidine, 16,16‐dimethyl prostaglandin E2 16,16 DMPGE2), or omeprazole. Single asterisk, P < 0.05; double asterisk, P <0.01.

From Konturek 93


Figure 4.

Mean acid outputs from Heidenhain pouch, HP, in response to graded doses of intravenous pentagastrin, histamine, or 15% liver extract meal, LE, before, pre‐op, and after, post‐op, excision of fundic mucosa.

From Soon‐Shiong and Debas 197. Copyright 1980 by The American Gastroenterological Association


Figure 5.

Responses to 300‐ml liquid meal of 15% liver extract in control stage, C, after truncal vagotomy, AV, and after proximal gastric vagotomy, PGV. A: plasma gastrin increment over basal aftermeal (n = 6 dogs); B: first 4‐h gastric fistula acid output in response to meal (n = 6 dogs); C: Heidenhain pouch acid output in response to meal in three stages (n = 3 dogs).

From Debas et al. 27


Figure 6.

Effects of distension of vagally innervated antral pouch with 100 mM NaHCO3 or 100 mM HCl on acid output from vagally innervated gastric fistula and on increments in serum gastrin concentrations. Acidification of antral pouch abolished gastrin release but only moderately reduced acid output, indicating that pylorooxyntic reflex was operating. Vagal denervation of antral pouch abolished the effect.

From Debas et al. 28


Figure 7.

Mean serum gastrin level (top) and gastric acid secretion (bottom) in response to amino acid meal of varying pH in duodenal ulcer, DU, (n = 9) and normal subjects (n = 12). Single asterisk, significant increase above basal levels; double asterisk, significant difference between duodenal ulcer and normal subjects; triple asterisk, significantly less than peak.

From Thompson and Swierczek 217


Figure 8.

Effect of acidification of duodenal bulb before and after separation from pylorus or of exogenous secretin infused in small (.2 U·kg‐1·h‐1) and large 1.6 U·kg‐1·h‐1) doses on gastric acid secretion from gastric fistula and on plasma secretin levels.

Adapted from Konturek and Johnson 112


Figure 9.

Effects of immunoneutralization of circulating secretin on serum gastrin and gastric acid responses to 5% liver extract, LE, meals in stomach adjusted to pHs varying from 7.0 to 2.0 or to 5% liver extract meal of pH 7.0 combined with intravenous infusion of graded doses of secretin (.03 ‐ 2.0 U·kg‐1·h‐1). Mean ± SE of 10 tests on 5 dogs with gastric and pancreatic fistulas. Secretin antiserum almost completely removed circulating secretin both in tests with meals of varying pH and exogenous secretin. Single asterisk, signifcantly different from control.

From Konturek et al. 105


Figure 10.

Effects of intravenous infusion of exogenous gastric inhibiting peptide, GIP, 1.0 μg·kg‐1·h‐1) or fat administered intraduodenally or intravenously on gastric acid secretion from Heidenhain pouch and gastric fistula stimulated by liver extract meal of pH 5.5 in main stomach (left) and serum GIP and gastrin levels (right) in dogs. Mean ± SE of 6 tests or 6 dogs. Single asterisk, significantly different from control.

From Konturek et al. 113


Figure 11.

Gastric acid and plasma neurotensin concentration during infusion of pentagastrin 150 ng·kg‐1·h‐1) and neurotensin (500 ng·kg‐1·h‐1) in 7 duodenal ulcer patients before (A) and after (B) parietal cell vagotomy.

From Olsen et al. 156


Figure 12.

Effect of epidermal growth factor (EGF) 1.0 μg·kg‐1·h‐1) on acid secretion from gastric fistula and Heidenhain pouches stimulated by pentagastrin 2.0 μg·kg‐1·h‐1), histamine 40 μg·kg‐1·h‐1), or urecholine 100 μg·kg‐1·h‐1). Single asterisk, significantly different from control.

From Konturek at al. 102


Figure 13.

Inhibitory effects of gastrin‐releasing peptide (GRP) on gastric acid output in pylorus‐ligated rats stimulated by intracisternal thyrotropin‐releasing hormone (TRH), 2‐deoxy‐d‐glucose 2‐DG), or histamine (HIS) without and with intracisternal administration of GRP.

From Taché et al. 205. Copyright 1981 by The American Gastroenterological Association


Figure 14.

Model for regulation of gastrin and somatostatin release in antrum by cholinergic and noncholinergic (bombesinergic) intramural neurons. Somatostatin (SS) cell is shown structurally and functionally coupled to gastrin cell. Sensory bipolar neuron links the regulatory cholinergic (ACh) and bombesinergic (BOM) neurons to luminal stimulus. Luminal stimulus could act directly on gastrin and somatostatin cells.

From Saffouri et al. 176. Copyright 1984 by The American Gastroenterological Association
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Article Title: Inhibition of Gastric Acid Secretion
 

How to Cite

Stanisław J. Konturek. Inhibition of Gastric Acid Secretion. Compr Physiol 2011, Supplement 18: Handbook of Physiology, The Gastrointestinal System, Salivary, Gastric, Pancreatic, and Hepatobiliary Secretion: 159-184. First published in print 1989. doi: 10.1002/cphy.cp060309