Gastric sensitivity and reflexes: basic mechanisms underlying clinical problems
Related Experiment Video
Updated: May 5, 2026

Fabrication and Implantation of Miniature Dual-element Strain Gages for Measuring In Vivo Gastrointestinal Contractions in Rodents.
Published on: September 18, 2014
Fernando Azpiroz1, Christine Feinle-Bisset, David Grundy
1Digestive System Research Unit, Hospital General Vall d'Hebron, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd), 08035, Barcelona, Spain, azpiroz.fernando@gmail.com.
Abstract:
Both reflex and sensory mechanisms control the function of the stomach, and disturbances in these mechanisms may explain the pathophysiology of disorders of gastric function. The objective of this report is to perform a literature-based critical analysis of new, relevant or conflicting information on gastric sensitivity and reflexes, with particular emphasis on the comprehensive integration of basic and clinical research data. The stomach exerts both phasic and tonic muscular (contractile and relaxatory) activity. Gastric tone determines the capacity of the stomach and mediates both gastric accommodation to a meal as well as gastric emptying, by partial relaxation or progressive recontraction, respectively. Perception and reflex afferent pathways from the stomach are activated independently by specific stimuli, suggesting that the terminal nerve endings operate as specialized receptors. Particularly, perception appears to be related to stimulation of tension receptors, while the existence of volume receptors in the stomach is uncertain. Reliable techniques have been developed to measure gastric perception and reflexes both in experimental and clinical conditions, and have facilitated the identification of abnormal responses in patients with gastric disorders. Gastroparesis is characterised by impaired gastric tone and contractility, whereas patients with functional dyspepsia have impaired accommodation, associated with antral distention and increased gastric sensitivity. An integrated view of fragmented knowledge allows the design of pathophysiological models in an attempt to explain disorders of gastric function, and may facilitate the development of mechanistically orientated treatments.
Related Concept Videos
Gastroesophageal Reflux Disease II: Clinical Features and Management
Clinical Manifestations
GERD presents itself in a multitude of ways, with symptoms varying from person to person. The hallmark symptoms are...
Neural Regulation
Gastritis III: Clinical Manifestations and Management
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
Gastroesophageal Reflux Disease
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...
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...

