The mechanism by which gastric acid is secreted and how this secretion is neutralised in the small intestine - Essay Example

? THE MECHANISM BY WHICH GASTRIC ACID IS SECRETED AND HOW THIS SECRETION IS NEUTRALISED IN THE SMALL INTESTINE by of the of the Professor Name of the School City, State October 10, 2012 Human Beings are the only mammals that secrete hydrochloric acid during the fasting state. The secretion of Gastric acid is an intricate, well regulated process in which different specialized gastric and duodenal cells play a vital role. Its secretion is mediated through hormonal and neural pathways. Stimulation of the vagus nerve acts as the neural effector while histamine and gastrin act as the hormonal effectors. Gastric acid production is the physiologic function closely associated with the stomach. Food acts as a physiologic stimulus for the production of gastric acid. Although gastric acid is produced in response to a meal, it plays a rather small role in digestion. However, it still does play a role in digestion. The stomach on the other hand has a well developed mucosal defensive mechanism which protects it from caustic injury. Parietal cells which are responsible for creating this concentrated acid environment within the lumen of the stomach are located at the centre of this elaborate system. Figure 1: The parietal cell. Cited in Thomson Reuters, 1999. The parietal cell has special histamine receptors known as H2 receptors. The stimulation of these receptors leads to increased acid secretion. Enterochromaffinlike (ECL) cells are special neuroendocrine cells of the stomach accredited with the production of histamine.ECL cells are mainly located in acid-secreting regions of the stomach. Rhoades and Bell (2009, p.503) point out that “The mechanisms that stimulate the ECL cells to release histamine are poorly understood.” The importance of histamine as an effector of gastric acid secretion has been indirectly demonstrated by the effectiveness of cimetidine which is a H2 blocker in reducing the secretion of acid. Physiologic regulation of gastric acid secretion is controlled by three major stimulants namely; histamine, gastrin and acetylcholine. Parietal cells are innervated by intrinsic and extrinsic nerves of the parasympathetic nervous system. Gastrin is the primary endocrine stimulant of the parietal cell. It is synthesized, stored and secreted by G-cells of the antral mucosa. Endocrine cell activity is regulated by dietary or luminal nutrients, nerves and paracrine factors. With luminal acid being a potent physiologic inhibitor of hormone release, amino acids, peptides and amines are primary luminal stimulatory factors. Histamine acts on specific H2 receptors of the parietal cell. The H2 receptors subsequently activate adenylate cyclise through a G-protein linking mechanism. Raff (2003, p.166), states that this results in “an increase in cytoplasmic cAMP results in the activation of protein kinase A and phosphorylation of proteins that regulate the opening of CI- ion channels in the canalicular membrane.” Acetylcholine (Ach), released from vagus nerve terminals bind to muscarinic (M3) receptors and activates the parietal cell through the IP3-Ca++ pathway. Food stimulated increase in gastric acid secretion occurs in a sequential order divided into three main phases namely; cephalic phase, gastric phase and intestinal phase. Phase Stimulus Pathway Stimulus to Parietal Cell Cephalic Thought of food, smell, taste, chewing and swallowing. Vagus nerve to:Parietal cells G cells Acetylcholine (Ach), Gastrin Gastric Stomach distention Local (enteric) reflexes and vago-vagal reflexes to: Parietal cells G cells Acetylcholine (Ach), Gastrin Intestinal Protein digestion products in duodenum Amino acids in blood Amino acids Table 1: Cephalic, Gastric, and Intestinal phases of Stimulation of Acid Secretion after Ingesting a Meal. Cited in Rhoades and Bell, 2009, p.504. The cephalic phase is associated with the central nervous system. Smelling, chewing, swallowing or simply the thought of food sends impulses to the parietal and G cells in the stomach through the vagus nerves. The vagus nerve endings then release Acetylcholine (Ach), which directly stimulates the secretion of acid from parietal cells. Vagus nerves are also responsible for releasing gastrin-releasing peptide (GRP), which then stimulates G-cells to release gastrin. This also indirectly stimulates acid secretion by the parietal cell. The effect of GRP is atropine-resistant showing that it works through a non-cholinergic pathway. 40 percent of total acid secretion occurs during the cephalic phase. The Gastric phase results from gastric distention and chemical agents for example digested proteins. Other chemicals like alcohol and caffeine also stimulate the secretion of gastric acid although the mechanisms are not well understood. Rhoades and Bell (2009, p.504) state that “Distension of the stomach stimulates mechanoreceptors, which stimulate the parietal cells directly through short local (enteric) reflexes and by long vago-vagal reflexes.” Vago-vagal reflexes are mediated by afferent and efferent impulses travelling in the vagus nerves. Digested proteins present in the stomach also stimulate gastric acid secretion through the mediation of gastrin release. 50 percent of total gastric acid secretion occurs during the gastric phase. The intestinal phase results from protein digestion products in the duodenum; this happens through the action of circulating amino acids on the parietal cells. Distention of the small intestine which may occur through the release of entero-oxyntin hormone for the intestinal endocrine cells also stimulates acid secretion. 10 percent of total gastric acid secretion occurs during the intestinal phase. Figure 2: Gastric acid secretion process. Cited in jpp, n.d. The secretion of gastric acid is inhibited by gastric hormones. Inhibition of gastric acid secretion is of physiological importance for two reasons. The first reason is because the secretion of gastric acid is only vital during food digestion. Secondly, the presence of too much gastric acid can cause damage to the gastric and duodenal mucosal surfaces and this could lead to conditions related to ulcers. Gastric luminal PH regulates gastric acid secretion. Acidification of the duodenal lumen also inhibits gastric acid secretion. This is because acidification causes the release of secretin responsible for inhibiting the release of gastrin and other peptides known as entero-gastrones. These peptides are released by the intestinal endocrine cells. Fatty acids, acid and hyperosmolar solutions in the duodenum stimulate enterogastrones release whish consequently inhibits gastric acid secretion. An enterogastrone known as gastric inhibitory peptide produced by the endocrine cells of the small intestine inhibit acid secretion by the parietal cell. Gastric acid secretion plays a significant role in the human stomach. Although it plays a small role in digestion, it is an essential component of digestion. Research has shown that gastric acid provides primary defence against enteric infection. This is because it kills majority of bacteria ingested into the stomach. Reference List Konturek, S.J. et al., n.d. Helicobacter Pylori and Its Involvement in Gastritis and Peptic Ulcer Formation. 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