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Background: It is well established that the esophageal distention leads to gastric relaxation, partly by vago-vagal reflex but till now, the effect of esophageal distention on gastric acid secretion has not been investigated. The aim of this study was to investigate the effect of esophageal distention (ED) on basal and stimulated gastric acid secretion. Methods: Adult male Wistar rats (200-240g) were deprived of food but not water for 24 hrs before the experiments. Under urethane anesthesia (1.2 g/kg, i.p.), animals underwent tracheostomy and laparotomy. A catheter was inserted in the stomach through duodenum for gastric distention and gastric washout and the esophagus was cannulated with a distensible balloon orally to distend esophagus (0.3 ml, 10 min). Gastric acid secretion was stimulated by gastric distention, carbachol (4 µg/kg, i.p.) or histamine (5 mg/kg, s.c.). Effects of vagotomy, L-NAME (10 mg/kg, i.v.), L-arginine (500 mg/kg, i.p.) and hexamethonium were also investigated. Results: Esophageal distention reduces basal and gastric distention, carbachol and histamine stimulated acid secretion (P

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Background and Aim H2S is an important gasotransmitter in the gastrointestinal tract. The aim of the present study was to investigate the effect of exogenous H2S on gastric acid secretion. Methods Male Wistar rats were randomly divided into physiological saline (PS) group, sodium hydrosulfide (NaHS; 50, 100, and 150 µmol/kg body weight) group, glibenclamide + NaHS group, and SQ22536 + NaHS group. PH of gastric juice before injection and after injection were determined by a PH meter. Results The results showed that NaHS, an exogenous H2S donor, injected into the enterocoelia significantly reduced the PH of gastric juice, the same volume of PS administered similarly did not change PH of gastric juice, the promotional effect of NaHS on gastric acid secretion could be abolished by glibenclamide, an ATP-sensitive potassium channel K(ATP) blocker SQ22536, an inhibitor of adenyl cyclase. Conclusions The data from these experiments suggest that exogenous H2S promoted gastric acid secretion, which may occur via K(ATP) channels and activate AC-cAMP pathway. [ABSTRACT FROM AUTHOR]

Gastric acid secretion levels are an important determinant of the manifestation of acid-related upper GI diseases such as gastroesophageal reflux disease. We recently reported that gastric acid secretion levels did not change from the 1990s to 2010s in H. pylori-negative asymptomatic Japanese outpatients with a mean age of 63 years old. However, because young people have a quite different lifestyle, including dietary pattern, from elderly people in Japan, it is worth investigating any chronologic changes in gastric acid secretion in younger generations. The aim of this analysis is to investigate the potential changes in gastric acid secretion from 1995 to 2014 in young Japanese healthy volunteers. Eighty-eight young Japanese healthy volunteers under the age of 40 with a mean age of 26 were extracted from a database accumulated from 1995 to 2014 for the present analysis. Their gastrin-stimulated gastric acid level was determined with the endoscopic gastrin test. In 76 H. pylori-negative subjects, gastric acid secretion levels showed a significant positive correlation with the calendar year when the test was performed (r = 0.27, p < 0.01). A similar trend was observed in 12 H. pylori-positive subjects. A chronological 5-year time period showed a significant positive association with gastric acid secretion in univariate and multivariate analyses (p < 0.01 and p = 0.01, respectively). Gastric acid secretion levels have been increasing in young Japanese healthy volunteers during the last 20 years. We need to monitor future trends in the prevalence of acid-related diseases such as gastro-esophageal reflux disease in Japan. [ABSTRACT FROM AUTHOR]

There are several studies on the gastroprotective effect of Zingiber officinale, however, the nature of this effect has not been fully elucidated. In the present study, the gastroprotective activity and the underlying mechanism of the 95% ethanolic extract of Z. officinale was investigated. The extract was evaluated against gastric ulceration induced either by hydrochloric acid (HCl) or water immersion restraint stress (WIR) or aspirin (ASP). Pretreatment with the extract (0.1, 0.25, 0.5 or 1.0 g/kg) for 30 minutes before inducing an ulcer by HCl, WIR and ASP decreased gastric lesions with maximal inhibitions of 81.7, 44.1 and 68.2%, respectively. Moreover, the involvement of gastric secretion on this antigastric ulcer activity was determined in a model of histamine-induced secretion in gastric fistulae of rats. The extract significantly increased visible gastric mucus secretion and had a tendency to increase the secretory rate of soluble gastric mucus. Nevertheless, it had no effect on gastric pH, acid and pepsin secretion. These results demonstrate that the Z. officinale extract exerts moderate gastric ulcer protection by increasing gastric mucus secretion. [ABSTRACT FROM AUTHOR]

Purpose – The purpose of this paper is to study the effect of chronic consumption of fresh palm oil (FPO) and thermoxidized palm oil (TPO) diet on gastric acid secretion, pepsin secretions, gastric mucus output and gastric cytoprotection. Design/methodology/approach – Adult Wistar rats were randomly assigned into three groups, i.e. control, FPO and TPO groups (n = 10 in each). The control group was fed with normal rat chow only, the FPO group was fed on diet containing 15 per cent v/w FPO and the TPO group was fed with diet containing v/w of thermally oxidized palm oil. All animals had free access to feed and water, and the feeding lasted for 14 weeks. At the end of the feeding period, gastric acid secretion, pepsin secretion, mucus output and gastric ulceration were measured following standard methods. Findings – There was increase in histamine-stimulated gastric acid output in the TPO diet-fed group (p < 0.01) compared with the control and FPO diet-fed groups. No significant change in the mucus output was observed across all the experimental groups; whereas, pepsin secretion was significantly higher (p < 0.05) in the TPO diet-fed group (0.46 ± 0.27) compared with the control (0.14 ± 0.05) and FPO diet-fed groups (0.25 ± 0.01). Ulcer scores in the TPO diet-fed group (15.5 ± 0.33) was significantly higher (p < 0.01) compared with the control (10.0 ± 0.05) and FPO diet-fed (5.0 ± 0.04) groups. Originality/value – Chronic consumption of TPO increased gastric acid and pepsin secretion (gastric-aggressive factors) without a change in the mucus output. This can bring about gastric ulceration; therefore, the liberal use of TPO should be discouraged. [ABSTRACT FROM AUTHOR]

Adenosine modulates different functional activities in many cells of the gastrointestinal tract; some of them are believed to be mediated by interaction with its four G protein-coupled receptors. The renewed interest in the adenosine A2B receptor (A2BR) subtype can be traced by studies in which the introduction of new genetic and chemical tools has widened the pharmacological and structural knowledge of this receptor as well as its potential therapeutic use in cancer and inflammation- or hypoxia-related pathologies. In the acid-secreting parietal cells of the gastric mucosa, the use of various radioligands for adenosine receptors suggested the presence of the A2 adenosine receptor subtype(s) on the cell surface. Recently, we confirmed A2BR expression in native, nontransformed parietal cells at rest by using flow cytometry and confocal microscopy. In this study, we show that A2BR is functional in primary rabbit gastric parietal cells, as indicated by the fact that agonist binding to A2BR increased adenylate cyclase activity and acid production. In addition, both acid production and radioligand binding of adenosine analogs to isolated cell membranes were potently blocked by selective A2BR antagonists, whereas ligands for A1, A2A, and A3 adenosine receptors failed to abolish activation. We conclude that rabbit gastric parietal cells possess functional A2BR proteins that are coupled to Gs and stimulate HCl production upon activation. Whether adenosine- and A2BR-mediated functional responses play a role in human gastric pathophysiology is yet to be elucidated. [ABSTRACT FROM AUTHOR]