Disease relevance of Gastric Acid

• We conclude that most patients with duodenal ulcer disease have decreased proximal duodenal mucosal bicarbonate production at rest, in response to hydrochloric acid, and in relation to peak gastric acid secretion [1].
• Single intravenous infusions of 2A11 (20 mg/20-25-kg dogs) into normal mongrel dogs with surgically created gastric fistulas antagonized the stimulatory effects of exogenously infused gastrin-releasing peptide or bombesin on plasma gastrin release and gastric acid secretion [2].
• A large dose of cimetidine, which markedly reduced gastric acid secretion, had no effect on calcium absorption in normal subjects, and an achlorhydric patient with pernicious anemia absorbed calcium normally [3].
• In rats with chronic gastric fistula, constant infusion of somatostatin failed to maintain a sustained inhibition of basal and pentagastrin-stimulated gastric acid secretion for greater than 4-6 h [4].
• This study demonstrates that a continuous i.v. infusion of cimetidine adequately inhibits gastric acid hypersecretion in patients with Zollinger-Ellison syndrome [5].

Psychiatry related information on Gastric Acid

• The Japanese Mazindol study group investigated the action of an anorexiant, mazindol, and found that it reduced food intake by directly suppressing neurons in the lateral hypothalamus, inhibited gastric acid secretion, increased motor activity, decreased glucose absorption, and inhibited insulin secretion [6].
• In addition to measurements of gastric acid secretion after fasting and following histamine provocation, psychological ratings (Hamilton Anxiety Rating Scale and Zung Self-Assessment Scale for Anxiety) were carried out [7].

High impact information on Gastric Acid

• A tyrosine-based signal targets H/K-ATPase to a regulated compartment and is required for the cessation of gastric acid secretion [8].
• The fractions from these six patients also reduced gastrin-stimulated [14C]aminopyrine uptake by gastric cells (an index of gastric acid secretory activity in vitro) by 50.2 +/- 8.4 per cent (mean +/- S.D.), as compared with 9.2 +/- 4.1 per cent for the controls [9].
• In five patients ingestion of 80 mg of omeprazole inhibited gastric acid secretion by 26 to 100 per cent after 6 hours and by 76 to 100 per cent after 24 hours [10].
• Effect of low-dose propantheline on food-stimulated gastric acid secretion: comparison with an "optimal effective dose" and interaction with cimetidine [11].
• Inhibition of meal-stimualted gastric acid secretion showed a significant relation to peak blood cimetidine concentration (r is equal to 0.76, P less than 0.01) [12].

Chemical compound and disease context of Gastric Acid

• We investigated the influence of stress on gastric acid and duodenal HCO3- secretion in rats, and examined whether duodenal ulcers develop in rats under stress conditions in the absence or presence of acid hypersecretion caused by histamine [13].
• Omeprazole is a highly effective inhibitor of gastric acid secretion in patients with Zollinger-Ellison syndrome [14].
• A significant correlation was shown between the daily ranitidine dose required to eliminate symptoms and the pretreatment basal acid output (r = 0.81, p less than 0.001); gastric acid output had to be almost totally suppressed (i.e., less than 1 mEq/h) for pyrosis to disappear completely [15].
• A single administration of prostaglandin E2 (1 or 3 mg/kg) significantly reduced histamine-stimulated gastric acid secretion for 4 h in acute fistula rats with 1- or 2-wk-old ulcers, treated with or without daily indomethacin (1 mg/kg) [16].
• It is presumed that this prostaglandin may not have sufficient duodenal cytoprotective capacity to effectively heal duodenal ulcers, or that some suppression of gastric acid secretion may be required to achieve significant clinical efficacy [17].

Biological context of Gastric Acid

• These findings suggest a defect in autoregulation of gastrin release and gastric acid secretion at low pH in ulcer patients which may play a role in pathogenesis of this disease [18].
• Taken together, these results suggest a physiologic role for TFF2 to promote mucosal healing through the stimulation of proliferation and downregulation of gastric acid secretion [19].
• Intracisternal injection of calcitonin at 0.01 microgram inhibited gastric acid output by 90% in pylorus-ligated rats and suppressed gastric emptying of a liquid meal by 63%-94% in doses ranging from 0.01 to 5 micrograms [20].
• Cytoprotection by prostaglandins is unrelated to the inhibition of gastric acid secretion since, (a) it is maximal at doses that have no effect on gastric secretion, and (b) anti-secretory compounds (cimetidine, methscopolamine bromide) and antacids are not cytoprotective [21].
• Acutely administered caffeine modestly increases blood pressure, plasma catecholamine levels, plasma renin activity, serum free fatty acid levels, urine production, and gastric acid secretion [22].

Anatomical context of Gastric Acid

• Gastric acid secretion and lower-esophageal-sphincter pressure in response to coffee and caffeine [23].
• Somatostatin, a tetradecapeptide with potent inhibitory actions on gastric acid secretion, potentiated carbamylcholine-induced synthesis and release of prostaglandin E2 from isolated perfused rat stomachs [24].
• Antral somatostatin D cells probably act as chemoreceptors for gastric acid to mediate a paracrine inhibition on gastrin secretion from adjacent G cells [25].
• The results support the role of intracellular bicarbonate in the protection of duodenal epithelial cells from luminal gastric acid [26].
• The evidence suggests that cimetidine inhibits gastric acid secretion through blockade of histamine H2-receptors in the gastric mucosa [27].

Associations of Gastric Acid with chemical compounds

• We compared the dose-response relations of caffeine, regular coffee and decaffeinated coffee for gastric acid secretion and sphincter pressure in normal subjects [23].
• We report here that thyrotropin-releasing hormone (TRH) acts within the CNS to elicit a vagus-dependent stimulation of gastric acid secretion [28].
• Intrahypothalamic injections of 100 picomoles of pentagastrin or natural gastrin promptly increased secretion of gastric acid in conscious rats [29].
• Gastric acid secretion has been thought to depend on histamine stimulation of the parietal cell [30].
• Parenteral and intracerebroventricular administration of calcitonin in rats resulted in the suppression of gastric acid secretion [31].

Gene context of Gastric Acid

• Cholecystokinin is a negative regulator of gastric acid secretion and postprandial release of gastrin in humans [32].
• BACKGROUND: Both secretin and cholecystokinin (CCK) inhibit gastric acid secretion [33].
• Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice [34].
• CONCLUSIONS: These results indicate that sst2 is the main subtype whereby endogenous somatostatin suppresses gastric acid secretion through inhibition of gastrin action [35].
• The cardiac K+ channel KCNQ1 is essential for gastric acid secretion [36].

Analytical, diagnostic and therapeutic context of Gastric Acid

• Intravenous infusion of phenylalanine and tryptophan significantly stimulated gastric acid secretion to 50 and 52%, respectively, of the acid secretory response to intragastric peptone [37].
• Increased sensitivity of gastric acid secretion to gastrin in cirrhotic patients with portacaval shunt [38].
• Vagotomy blocked the effect of ICV NPY on gastric acid secretion in a urethane-anesthetized rat model with acute gastric fistula [39].
• In vivo, it is a potent inhibitor of histamine-stimulated gastric acid secretion in rats and dogs after both intravenous and oral administration [27].
• Intravenous injection of valosin (0.125-1 microgram/kg) dose-dependently increased gastric acid secretion 80-fold over basal, corresponding to 18% of the maximal pentagastrin-induced effect [40].

References