The regulation of acid and pepsin secretion reflects an intricate balance of chemotransmitters delivered to the gastric mucosa by several pathways that mediate both stimulatory and inhibitory mechanisms. Similarly, several mechanisms contribute to the remarkable ability of normal gastroduodenal mucosa to defend itself against injury from the acid/peptic activity in gastric juice and to rapidly repair injury when it does occur. Secretory, defense, and healing mechanisms are regulated by the same type of overlapping neural, endocrine, paracrine, and autocrine control pathways.
The numerous stimulators and inhibitors of each regulated element suggest redundant control; however, there is limited understanding of the actual physiologic and pathophysiologic importance of most of these pathways and chemotransmitters. The problem is that there remains a limited set of pharmacologic and molecular biologic tools to dissect the significance of each pathway.
Although gastric acid is not essential for life, the universal preservation of gastric acid secretion among vertebrates indicates critical evolutionary advantage. The benefits of gastric acid are to facilitate digestion of proteins and the absorption of calcium, iron, and vitamin B12. It also suppresses growth of bacteria, which can help prevent enteric infections and small intestinal bacterial overgrowth.
The physiologic stimulation of acid secretion has classically been divided into three interrelated phases: cephalic, gastric, and intestinal.
- The cephalic phase is activated by the thought, taste, smell and site of food, and swallowing. It is mediated mostly by cholinergic/vagal mechanisms.
- The gastric phase is due to the chemical effects of food and distension of the stomach. Gastrin appears to be the major mediator since the response to food is largely inhibited by immunoneutralizing or blocking gastrin action at its receptors.
- The intestinal phase accounts for only a small proportion of the acid secretory response to a meal; its mediators remain controversial.
http://tube.medchrome.com/2011/07/gastric-acid-secretion-physiology.html
Recent Advances in the Physiology of Gastric Acid Secretion
by BERNARD J. F. PEREY, M.D., F.R.C.S. [C], Montreal
ABSTRACT
The classic scheme of gastric acid secretion which divided the digestive period into cephalic, gastric and antral phases has become obsolete in the last 10 years. These "phases" are now seen as concurrently acting mechanisms which depend upon one another to be fully efficient. About half of all gastrin released during a meal is dependent upon vagal stimulation of the antrum.
Also, vagotomny desensitizes the acid-secreting parietal cells to the effect of all other types of stimuli.
The number of parietal cells (parietal cell mass) varies greatly according to the gastric secretory activity of each individual. It is highest with duodenal ulcer and lowest with gastric ulcer.
Parietal cell hyperplasia or atrophy can be induced experimentally, but the factors controlling the size of the parietal cell mass in man have not been studied.
A scheme of acid secretion which incorporates recent advances is presented.
To read the the full text please visit
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1922094/pdf/canmedaj01025-0026.pdf
Pathogenesis of Gastro-Esophageal Reflux Disease: What role do Helicobacter pylori and host genetic factors play?
by Dipti Chourasia, Uday C Ghoshal
Department of Gastroenterology,
Sanjay Gandhi Postgraduate Institute of Medical Sciences,
Raebareli Road,
Lucknow 226014, India;
Abstract
Gastro-oesophageal reflux disease is a multifactorial disease. The roles of environmental, dietary, and host physiological factors are well established. However, the plausible role of Helicobacter pylori infection in gastro-oesophageal reflux disease is still controversial. Furthermore, the role of host genetic factors remains unidentified. Extensive PubMed review of the previous literature has revealed that H. pylori may be negatively associated with gastro-oesophageal reflux disease. Ethnic or inter-individual variations in response to H. pylori infection may also determine disease outcome. Thus, host genetic factors may play an important role in deciding the final outcome of disease. Limited studies have shown that homEM of CYP2C19, b allele (val105) of GSTP1, T allele of IL1B-31, 2/2 genotype of IL1RN +2018, 2/2 genotype of IL-10 -1082, A/A genotype of CCND1 G870A, and homozygous variant of XPC PAT gene are potential risk factors for the development of gastro-oesophageal reflux disease or its complications such as Barrett’s oesophagus and oesophageal adenocarcinoma. There is scant data on the relationship between gastro-oesophageal reflux disease and H. pylori in India, and therefore, further studies are directly required to explore this issue.
To read the the full text please visit
http://www.tropicalgastro.com/articles/29/1/Pathogenesis-of-gastro-oesophageal-reflux-disease-what-role-do-Helicobacter-pylori-and-host-genetic-factors-play.html
Pathogenesis of Gastro-Esophageal Reflux Disease: What role do Helicobacter pylori and host genetic factors play?
by Dipti Chourasia, Uday C Ghoshal
Department of Gastroenterology,
Sanjay Gandhi Postgraduate Institute of Medical Sciences,
Raebareli Road,
Lucknow 226014, India;
Abstract
Gastro-oesophageal reflux disease is a multifactorial disease. The roles of environmental, dietary, and host physiological factors are well established. However, the plausible role of Helicobacter pylori infection in gastro-oesophageal reflux disease is still controversial. Furthermore, the role of host genetic factors remains unidentified. Extensive PubMed review of the previous literature has revealed that H. pylori may be negatively associated with gastro-oesophageal reflux disease. Ethnic or inter-individual variations in response to H. pylori infection may also determine disease outcome. Thus, host genetic factors may play an important role in deciding the final outcome of disease. Limited studies have shown that homEM of CYP2C19, b allele (val105) of GSTP1, T allele of IL1B-31, 2/2 genotype of IL1RN +2018, 2/2 genotype of IL-10 -1082, A/A genotype of CCND1 G870A, and homozygous variant of XPC PAT gene are potential risk factors for the development of gastro-oesophageal reflux disease or its complications such as Barrett’s oesophagus and oesophageal adenocarcinoma. There is scant data on the relationship between gastro-oesophageal reflux disease and H. pylori in India, and therefore, further studies are directly required to explore this issue.
To read the the full text please visit
http://www.tropicalgastro.com/articles/29/1/Pathogenesis-of-gastro-oesophageal-reflux-disease-what-role-do-Helicobacter-pylori-and-host-genetic-factors-play.html
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