Related Experiment Video
Updated: Jul 20, 2026

Fabrication and Implantation of Miniature Dual-element Strain Gages for Measuring In Vivo Gastrointestinal Contractions in Rodents.
Published on: September 18, 2014
Pyloric antral inhibition of gastrin release
1Creighton University, School of Medicine, Department of Physiology, Omaha, Nebraska 68178, USA.
Abstract:
Inconsistencies and omissions in current explanations for the well known depressions of gastric acid secretion and blood gastrin levels following acidification by antral stimulants are discussed. Evidence is presented which favors a reciprocal sensitivity relationship between the fundic mucosa and the antral G cells, such that blood gastrin levels rise when the secreting fundic mucosa is compromised and acid secretion in response to exogenous gastrin is increased when G cells are depressed or reduced. The functional connections between the two phenomena are considered to be nervous.
Related Concept Videos
Hormonal Regulation
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
Intestinal Phase of Digestion
The arrival of the chyme in the small intestine distends the duodenum, which triggers the enterogastric reflex. This distension...
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology

