The Relation between Basal Gastric pH and Serum Gastrin

Bins, M.; Burgers, P. I. C. J.; Selbach, Stephanie; Wettum, T. B. Van; Lamers, C. B. H. W.; Tongeren, J. H. M. Van

doi:10.1159/000198761

Cited by 19 publications

(7 citation statements)

References 7 publications

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“…Gastrin acts on the gastrin (CCK‐2) receptor on the so‐called ECL cells in the gastric oxyntic mucosa (Sandvik & Waldum 1991; Ding et al 1997; Bakke et al 2001) stimulating histamine release from these cells (Sandvik et al 1987; Sandvik & Waldum 1991; Prinz et al 1993; Chen et al 1994). Histamine, in turn, binds to H 2 receptors on the parietal cell (Black et al 1972) and stimulates acid secretion. The release of gastrin is under control of gastric acidity which has a negative feedback on the G cell.…”

Section: Regulation Of Gastric Acid Secretionmentioning

confidence: 99%

Rebound Hypersecretion after Inhibition of Gastric Acid Secretion

Qvigstad

Waldum

2004

Basic Clin Pharma Tox

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Drugs inhibiting gastric acid secretion are widely used because of the high prevalence of acid-related disorders. However, from clinical experience it seems that symptom relapse is common after withdrawal of these drugs. Experimental as well as clinical studies have demonstrated an increased acid secretion after a period of treatment with either histamine 2 receptor antagonists or proton pump inhibitors. Rebound hypersecretion is likely to reflect the following sequence of events: Long-term inhibition of acid output is accompanied by elevated serum gastrin levels, leading to enterochromaffinlike cell activation and proliferation, resulting in increased amounts of histamine being mobilized from these cells to stimulate the parietal cells. The clinical consequences of rebound hypersecretion have not been settled.

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Section: Regulation Of Gastric Acid Secretionmentioning

confidence: 99%

Rebound Hypersecretion after Inhibition of Gastric Acid Secretion

Qvigstad

Waldum

2004

Basic Clin Pharma Tox

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“…The numbers of antral gastrin cells were doubled and the numbers of antral somatostatin cells half that in the controls. These results show that long-standing lansoprazole-evoked hypergastrinemia affects the ECL cell similarly to omeprazole, ranitidine and other acid secretion inhibitors.Inhibition of gastric acid secretion raises the concentration of plasma gastrin, which is secreted from antral gastrin cells [1]. Gastrin stimulates the proliferation of the entrochromaffin-like (ECL) cells [2,3], which are the major histamine-producing and histamine storing cells in the rat stomach [4,5], A sus tained hypergastrinemia, secondary to inhibi tion of gastric acid secretion, results in hyper plasia of ECL cells [6,7], Long-term (2 years…”

mentioning

confidence: 99%

Lansoprazole and Omeprazole Have Similar Effects on Plasma Gastrin Levels, Enterochromaffin-Like Cells, Gastrin Cells and Somatostatin Cells in the Rat Stomach

et al. 1992

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This study compares the effects of lansoprazole and omeprazole on the activation and proliferation of enterochromaffin-like (ECL) cells in the rat stomach. Lansoprazole was given orally once daily for 10 weeks in two doses, 135 and 200 μmol/kg. Omeprazole was given by the same regimen in a dose of 400 μmol/kg, which is equipotent in terms of acid inhibition to the higher lansoprazole dose. Lansoprazole (both doses) as well as omeprazole raised the plasma gastrin levels about 11 -fold 2 h after dosing and 8- to 10-fold 24 h after dosing, reflecting complete (2 h) and 70-80% (24 h) reductions of gastric acid secretion. Administration of either drug for 10 weeks increased the weight of the stomach and the oxyntic mucosa. The oxyntic mucosal histidine decarboxylase activity, histamine concentration and ECL cell density were increased to the same extent in the rats given either of the two lansoprazole doses or omeprazole. The numbers of antral gastrin cells were doubled and the numbers of antral somatostatin cells half that in the controls. These results show that long-standing lansoprazole-evoked hypergastrinemia affects the ECL cell similarly to omeprazole, ranitidine and other acid secretion inhibitors.

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“…It is well-known that the pH of the antral content is one of the factors that regulates the release of gastrin from these cells. Thus, a low pH will inhibit and an elevated antral pH will increase the re lease of gastrin from the G cells into the blood [1][2][3]. Therefore, the plasma gastrin levels should be expected to increase during periods of sustained inhibition of gastric acid secretion.…”

mentioning

confidence: 99%

Effects of Omeprazole and Ranitidine on Gastric Acid Secretion, Blood Gastrin Levels and [<sup>3</sup>H]-Thymidine Incorporation in the Oxyntic Mucosa from Dogs and Rats

Ryberg¹,

Mattsson²,

Carlsson³

1988

Digestion

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Dogs provided with a gastric fistula were treated orally for 1 week either with the H⁺, K⁺-ATPase inhibitor omeprazole, 80 μmol/kg once daily, or with the histamine H₂ receptor antagonist ranitidine, 85–175 μmol/kg every 8 h. Acid secretion, serum gastrin levels and [³H]-thymidine incorporation in the corpus mucosa were determined before, during and after the treatment period. In order to examine differences between species, plasma gastrin levels and [³H]-thymidine incorporation in the oxyntic mucosa were also determined in female rats treated up to 1 week with omeprazole, 400 μmol/kg orally once daily. Histamine-stimulated gastric acid secretion in dogs treated with omeprazole or ranitidine was almost completely inhibited during the whole treatment period. As a consequence of that, the meal-stimulated gastrin levels were increased (7-fold) during treatment by both compounds. [³H]-thymidine incorporation in the dog corpus mucosa was increased approximately 4 times on day 5 both with omeprazole and ranitidine. After the treatment was stopped, gastric acid secretion, serum levels of gastrin and the rate of [³H]-thymidine incorporation were back to control level in both groups within 11 days. In the rats, the plasma gastrin levels increased 10-fold and the rate of [³H]-thymidine incorporation in the corpus mucosa increased 3-fold during treatment with omeprazole. In conclusion, a pronounced suppression of gastric acid secretion over the day with antisecretagogues results in hypergastrinemia in both dogs and rats. As a consequence of the trophic effect of gastrin, the incorporation of [3H]-thymidine in the oxyntic mucosa is increased. The results show that these effects are obtained regardless of the mechanism by which acid secretion is inhibited.

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The Relation between Basal Gastric pH and Serum Gastrin

Cited by 19 publications

References 7 publications

Rebound Hypersecretion after Inhibition of Gastric Acid Secretion

Rebound Hypersecretion after Inhibition of Gastric Acid Secretion

Lansoprazole and Omeprazole Have Similar Effects on Plasma Gastrin Levels, Enterochromaffin-Like Cells, Gastrin Cells and Somatostatin Cells in the Rat Stomach

Effects of Omeprazole and Ranitidine on Gastric Acid Secretion, Blood Gastrin Levels and [<sup>3</sup>H]-Thymidine Incorporation in the Oxyntic Mucosa from Dogs and Rats

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