Mental stress and gastric acid secretion
Their duration of action mirrors their plasma elimination half-lives, and is measured in a few hours. Large doses can produce marked inhibition of basal or stimulated acid secretion, although the effect quickly disappears.
Histamine secreted from nearby enterochromaffin-like (ECL) cells stimulates the parietal cells to secrete acid. A variety of substances can stimulate the ECL cell to secrete histamine. Histamine H 2 -receptors are located on the basolateral membranes of the acid-secreting parietal cells in the stomach. They are activated by histamine derived from neighbouring mucosal cells.
Below pH of 2, stomach acid inhibits the parietal cells and G cells; this is a negative feedback loop that winds down the gastric phase as the need for pepsin and HCl declines. Autonomic nervous system, the one that regulates breathing rate, heart rate and other physiological processes as a function of circadian time, regulates secretion of gastric acid. Vagus nerve, part of parasympathetic nervous system (the one responsible for “rest and digest” part of behavior, opposite to sympathetic “fight or flight”) stimulates secretion of gastric acid and regulated through circadian mechanism. While it might be premature to infer among snakes an adaptive interplay of tissue function, metabolism and feeding habits from this two-species study (Garland and Adolph, 1994), the scholarly study does encourage attention to the following questions. (1) What has been the target(s) of selection in the adaptive regulation of GI performance and metabolism for snakes?
Snakes exhibit an apparent dichotomy in the regulation of gastrointestinal (GI) performance with feeding and fasting; frequently feeding species modestly regulate intestinal function whereas infrequently feeding species rapidly upregulate and downregulate intestinal function with the start and completion of each meal, respectively. The downregulatory response with fasting for infrequently feeding snakes is hypothesized to be a selective attribute that reduces energy expenditure between meals.
A sample of gastric juice is aspirated. the antrum. The loss of parietal cells leads to achlorhydria (absent HCl production), and to deficiency of intrinsic factor. secretion of gastric juice means increased secretion of parietal cell juice.
INTRAVENOUS AMINO ACIDS STIMULATE GASTRIC ACID SECRETION IN INFANTS
In our study, both esomeprazole 20 mg q.d. and 20 mg b.i.d. achieved median gastric acid inhibition rate of 100% at steady state. The effect of increasing the dose and frequency of esomeprazole on gastric acid inhibition in this study corresponds with the results of previous western studies using 24-h pH monitoring. . Gastric acid inhibition rates in each subject at trough and steady states are indicated..
Some of the hormones that are released from the small intestine by products of digestion (especially fat), in particular glucagon and secretin, suppress acid secretion also. The release of histamine is the most important positive regulation mechanism of the secretion of gastric acid in the stomach. Its release is stimulated by acetylcholine and gastrin and inhibited by somatostatin.
Vasoactive intestinal peptide, cholecystokinin, and secretin all inhibit production. Diagram depicting the major determinants of gastric acid secretion, with inclusion of drug targets for peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD). The highly acidic environment in the stomach lumen causes proteins from food to lose their characteristic folded structure (or denature). This exposes the protein’s peptide bonds.