The vagus nerve mediates the neural regulation of gastric acid secretion in the gastric phase of a meal. Stimulation occurs in the cephalic and oral phases, leading to the secretion of acid from parietal cells and pepsinogen from chief cells. This initiates protein digestion when food reaches the stomach, generating protein hydrolysate and stimulating the secretion of gastrin from the gastric antrum mucosa. Additionally, gastric distention activates a vagovagal reflex, further stimulating the secretion of gastric acid and pepsinogen. Intrinsic neural pathways are also activated by distention, releasing acetylcholine from nerve terminals that activate cells in the gastric epithelium. Parietal cells express muscarinic receptors and secrete H+ in response to vagal efferent nerve activity. Parasympathetic activation releases gastrin from G cells in the gastric antrum via gastrin-releasing peptide from intrinsic neurons. Gastrin enters the bloodstream and stimulates the parietal cell to secrete H+ through an endocrine mechanism. Parietal cells express cholecystokinin type 2 (CCK2) receptors for gastrin. Vagal nerve stimulation also leads to the secretion of histamine, which potentiates the effects of gastrin and acetylcholine on parietal cells. Therefore, parasympathetic outflow to the stomach efficiently stimulates the parietal cell to secrete acid. In the gastric phase, vagovagal reflexes are activated by the presence of food in the stomach, resulting in secretion stimulation. Food in the stomach causes distention and stretch, detected by afferent nerve endings in the gastric wall, which transmit information to the brainstem and activate vagal efferent fibers, forming a vagovagal reflex. Additionally, the digestion of proteins increases the concentration of oligopeptides and free amino acids in the stomach lumen, which are detected by chemosensors in the gastric mucosa and also stimulate vagal afferent activity. The exact nature of these mechanisms is as follows:
• Fig.29.6Neural regulation of gastric acid secretion in the gastric phase of the meal is mediated by the vagus nerve. The stimulation that occurs in the cephalic and oral phases (before food reaches the stomach) results in stimulation of parietal cells to secrete acid and chief cells to secrete pepsinogen. Thus when food reaches the stomach, protein digestion is initiated by generating protein hydrolysate, which further stimulates secretion of gastrin from the mucosa of the gastric antrum. In addition, gastric distention activates a vagovagal reflex that further stimulates gastric acid and pepsinogen secretion. ˜ H+ ˜ Pepsinogen Endocrine (gastrin) Oligopeptides Protein Pepsin Pepsin pH 2.0 Pepsinogen ˜ H+ ˜ Pepsinogen ˜ Gastrin • Intrinsic neural pathways are also activated by distention Distention Dorsal vagal complex Neural (vagovagal) of acetylcholine from nerve terminals, which activates cells in the gastric epithelium. Parietal cells express muscarinic receptors and are activated to secrete H+ in response to vagal efferent nerve activity. In addition, parasympathetic activation, via gastrin-releasing peptide from intrinsic neurons, releases gastrin from G cells located in the gastric glands in the gastric antrum (see
Fig. 29.6 ). Gastrin enters the bloodstream and, via an endocrine mechanism, further stimulates the parietal cell to secrete H+ . Parietal cells express cholecystokinin type 2 (CCK2) receptors for gastrin. Histamine is also secreted in response to vagal nerve stimulation, and ECL cells express muscarinic and gastrin receptors. Thus gastrin and vagal efferent activity induce release of histamine, which potentiates the effects of both gastrin and acetylcholine on the parietal cell. Hence activation of parasympathetic (vagal) outflow to the stomach is very efficient at stimulating the parietal cell to secrete acid (
Fig. 29.7
In the gastric phase the presence of food in the stomach is detected and activates vagovagal reflexes to stimulate secretion. Food in the stomach results in distention and stretch, which are detected by afferent (or sensory) nerve endings in the gastric wall. These are the peripheral terminals of vagal afferent nerves that transmit information to the brainstem and thereby drive activity in vagal efferent fibers, a vagovagal reflex (see
Fig. 29.6 ). In addition, digestion of proteins increases the concentration of oligopeptides and free amino acids in the lumen, which are detected by chemosensors in the gastric mucosa. Oligopeptides and amino acids also stimulate vagal afferent activity. The exact nature of the