Gastric secretion is influenced by neural, hormonal, and local factors that operate during three overlapping phases: the cephalic, gastric, and intestinal phases.
Phases of Gastric Secretion and Influencing Factors
Here's a breakdown of the factors affecting gastric secretion during each phase:
1. Cephalic Phase
The cephalic phase prepares the stomach for the arrival of food. It's initiated by the sight, smell, taste, or thought of food.
- Neural Control:
- Vagus Nerve Stimulation: Sensory inputs activate the cerebral cortex and hypothalamus, which in turn stimulate the vagus nerve (cranial nerve X).
- Acetylcholine (ACh) Release: Vagal nerve endings release acetylcholine, directly stimulating parietal cells (to secrete HCl) and chief cells (to secrete pepsinogen).
- Gastrin-Releasing Peptide (GRP): Vagal stimulation also releases GRP, which stimulates G cells to release gastrin.
- Psychological Factors: Appetite and anticipation of a meal strongly influence this phase. Depression and loss of appetite can diminish gastric secretions.
2. Gastric Phase
The gastric phase begins when food actually enters the stomach.
- Gastric Distension: The physical stretching of the stomach wall activates mechanoreceptors. These receptors trigger:
- Vagovagal Reflexes: Local reflexes stimulate the vagus nerve, leading to ACh release and gastrin secretion (similar to the cephalic phase).
- Enteric Nervous System Activation: The enteric nervous system is also activated, further stimulating gastric secretions.
- Chemical Stimuli:
- Amino Acids and Peptides: The presence of partially digested proteins (peptides and amino acids) stimulates G cells to release gastrin.
- Caffeine and Alcohol: These substances can directly stimulate gastric acid secretion.
- pH Levels:
- Gastrin Regulation: Gastrin secretion is inhibited when the stomach pH falls below 2.0. This negative feedback mechanism prevents excessive acidity.
- Somatostatin Release: Low pH also stimulates the release of somatostatin from D cells in the stomach, which inhibits gastrin release, further reducing acid secretion.
3. Intestinal Phase
The intestinal phase controls gastric secretion as chyme enters the small intestine. This phase has both stimulatory and inhibitory components.
- Stimulatory Component:
- Intestinal Gastrin Release: Partially digested proteins in the duodenum can stimulate the release of a small amount of intestinal gastrin. This effect is relatively minor compared to gastric gastrin release.
- Inhibitory Component:
- Enterogastric Reflex: The presence of acidic chyme and partially digested fats in the duodenum triggers the enterogastric reflex, which inhibits gastric secretion and motility. This reflex is mediated by the enteric nervous system and vagal afferent fibers.
- Hormonal Inhibition:
- Secretin: Released by the duodenum in response to acidic chyme, secretin inhibits parietal cell secretion of HCl.
- Cholecystokinin (CCK): Released by the duodenum in response to fats and proteins, CCK inhibits gastric emptying and can reduce gastric secretion.
- Gastric Inhibitory Peptide (GIP) or Glucose-dependent Insulinotropic Peptide: Released in response to glucose and fats in the duodenum, GIP inhibits gastric acid secretion and promotes insulin release.
Summary Table of Factors Affecting Gastric Secretion
| Phase | Stimulatory Factors | Inhibitory Factors |
|---|---|---|
| Cephalic | Sight, smell, taste, thought of food, vagal stimulation | Depression, loss of appetite |
| Gastric | Gastric distension, peptides, amino acids, caffeine, alcohol | Low pH (below 2.0), Somatostatin release |
| Intestinal | Intestinal gastrin (minor) | Enterogastric reflex, Secretin, CCK, GIP |
In conclusion, gastric secretion is a complex process regulated by neural, hormonal, and local factors acting in concert during the cephalic, gastric, and intestinal phases. These factors ensure efficient digestion while preventing excessive acid secretion that could damage the gastrointestinal tract.
