Describe the regulation of gastric secretion
1. During the cephalic phase, the sight and smell of food stimulates parasympathetic fibers from the vagus nerve to stimulate gastric secretion and contraction. Chief cells are stimulated to release pepsinogen, while parietal cells are stimulated through ACh binding to muscarinic receptors to secrete HCl. The major mechanism for HCl secretion is indirect, through the vagus nerve stimulation of ECL cells and subsequent secretion of histamine, which in turn stimulates parietal cells to secrete HCl.
2. Food in the stomach: During the gastric phase, secretion of acid and pepsin is stimulated in response to two factors: (1) distension of the stomach by the volume of chyme; and (2) the chemical nature of the chyme. The presence of partially digested protein in the stomach lumen stimulates the chief cells to secrete pepsinogen and the G cells to secrete the hormone, gastrin. Gastrin, then is recirculated back to stimulate more pepsinogen and more HCl secretion (indirectly) creating a positive feedback loop. Fat inhibits acid secretion and glucose has no effect. As the pH of gastric juice drops, so does the secretion of gastrin and HCl release (perhaps mediated by the release of somatostatin from D cells). 3. During the intestinal phase, food is in the small intestine. Both neural reflexes from the duodenum in response to stretch and osmolality and a chemical hormone (enterogastrone, such as GIP, CCK and scretin) secreted by the duodenum appear involved in the inhibition of gastric secretion following a meal. This is to allow more time for the the small intestine to digest and absorb food in the chyme.