scholarly journals Role of ghrelin in the regulation of gastric acid secretion involving nitrergic mechanisms in rats

2008 ◽  
pp. 563-568
Author(s):  
HM Bilgin ◽  
C Tumer ◽  
H Diken ◽  
M Kelle ◽  
A Sermet
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Control Group ◽  
Albino Rats ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Plasma Nitrite

Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R), has been identified in the rat and human gastrointestinal tract. Ghrelin has been proposed to play a role in gastric acid secretion. Nitric oxide (NO) was shown as a mediator in the mechanism of ghrelin action on gastric acid secretory function. However, there is a little knowledge about this topic. We have investigated the role of ghrelin in gastric acid secretion and the role of NO as a mediator. Wistar albino rats were used in this study. The pyloric sphincter was ligated through a small midline incision. By the time, saline (0.5 ml, iv) was injected to the control group, ghrelin (20 μg/kg, iv) was injected to the first experimental group, ghrelin (20 μg/kg, iv) + L-NAME (70 mg/kg, sc) was injected to the second group and L-NAME (70 mg/kg, sc) was administered to the third group. The rats were killed 3 h after pylorus ligation; gastric acid secretion, mucus content and plasma nitrite levels were measured. Exogenous ghrelin administration increased gastric acid output, mucus content and total plasma nitrite levels, while these effects of ghrelin were inhibited by applying L-NAME. We can conclude that ghrelin participates in the regulation of gastric acid secretion through NO as a mediator.

scholarly journals Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole

Gut ◽  
1999 ◽  
Vol 44 (4) ◽  
pp. 468-475 ◽  
Author(s):  
D Gillen ◽  
A A Wirz ◽  
W D Neithercut ◽  
J E S Ardill ◽  
K E L McColl
Keyword(s):  
Helicobacter Pylori ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Intragastric Ph ◽  
Ammonia Production ◽  
Intragastric Acid ◽  
H Pylori

BACKGROUNDOmeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production byH pylori has been suggested as a probable mechanism.AIMSTo assess the effect ofH pylori status on gastric acid secretion during omeprazole treatment, and to examine the possible role of ammonia neutralisation of intragastric acid in increased omeprazole efficacy in infected subjects.METHODSTwentyH pylori positive and 12H pylori negative healthy volunteers were examined before and six to eight weeks after commencing omeprazole 40 mg/day. On both occasions plasma gastrin and acid output were measured basally and in response to increasing doses of gastrin 17 (G-17). Gastric juice ammonium concentrations were also measured.RESULTSPrior to omeprazole, measurements were similar in the H pyloripositive and negative subjects. During omeprazole, median basal intragastric pH was higher in the H pyloripositive (7.95) versus negative (3.75) subjects (p<0.002). During omeprazole basal, submaximal (180 pmol/kg/h G-17), and maximal acid outputs (800 pmol/kg/h G-17) were lower in H pylori positive subjects (0.0, 3.6, 6.0 mmol/h respectively) versus negative subjects (0.3, 14.2, 18.6 mmol/h) (p<0.03 for each). This effect was not explained by neutralisation by ammonia.CONCLUSIONThe presence ofH pylori infection leads to a more profound suppression of acid secretion during omeprazole treatment. The effect cannot be explained by neutralisation of intragastric acid by bacterial ammonia production and its precise mechanism has to be explained.

scholarly journals Antisecretory Effect of Hydrogen Sulfide on Gastric Acid Secretion and the Involvement of Nitric Oxide

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Seyyed Ali Mard ◽  
Hasan Askari ◽  
Niloofar Neisi ◽  
Ali Veisi
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Control Group ◽  
Antisecretory Effect ◽  
Cox 2 ◽  
Stimulation Of

The present study was designed to investigate the effect of H2S on distention-induced gastric acid secretion. Fifty-two rats were randomly assigned to seven experimental groups. The gastric acid secretion was stimulated by gastric distention. Two groups of rats received L-cysteine or saline for 5 days before stimulation of the gastric acid secretion. Two groups of animals also received NaHS or saline just prior to stimulation of the gastric acid secretion. The effect of L-NAME and propargylglycine was also investigated. The mucosal levels of the gene expression of cyclooxygenase-2 (COX-2), endothelial nitric oxide synthase (eNOS), and H+/K+-ATPaseα-subunit were quantified by qPCR and luminal concentrations of NO were determined. NaHS and L-cysteine decreased the gastric acid output in response to distention. The mRNA expression of H+/K+-ATPaseα-subunit decreased by NaHS and L-cysteine as compared with the control group while gene expression of eNOS and COX-2 was upregulated. The inhibitory effect of NaHS on distention-induced gastric acid secretion was mitigated by pretreatment of L-NAME. These findings suggest the involvement of NO in mediating the antisecretory effect of H2S.

Role of gastrin/CCK-B receptors in meal-stimulated acid secretion in rats

1997 ◽  
Vol 272 (5) ◽  
pp. G1243-G1248 ◽  
Author(s):  
K. Aurang ◽  
C. F. Spraggs ◽  
C. Jordan ◽  
K. C. Lloyd
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Rat Model ◽  
Acid Output ◽  
Male Rats ◽  
Plasma Histamine ◽  
Plasma Gastrin

Gastrin is the principal hormonal mediator of gastric acid secretion. Using an in vivo, intact, anesthetized rat model, we studied the role of gastrin/cholecystokinin (CCK)-B receptors in regulating the release of histamine and somatostatin during intragastric stimulation of acid secretion during a peptone meal. In pylorusligated, adult male rats (each implanted with a gastric cannula and portal venous and splenic artery catheters), after a 30-min basal period, gastric acid secretion was stimulated for 90 min either by an intravenous infusion of gastrin-17 (15 micrograms.kg-1.h-1) or by extragastric titration of 5 ml 8% peptone meal at pH 5.5. Basal and stimulated acid outputs and portal venous plasma gastrin, histamine, and somatostatin concentrations were measured before and after close-arterial injection of a new, relatively selective, gastrin/CCK-B receptor antagonist GR143330X. GR143330X reduced basal acid output by 50% but not basal plasma gastrin, histamine, or somatostatin concentrations. GR143330X reduced gastrin-stimulated acid output by 80%, plasma histamine by 70%, and plasma somatostatin by 34%. During intragastric peptone meal stimulation GR143330X reduced the acid response by 42% during the 30- to 60-min period but not during the 60- to 90-min period. GR143330X reduced the plasma histamine response by 72 and 68%, and the plasma somatostatin response by 32 and 54% during the 30- to 60- and 60- to 90-min periods, respectively. GR143330X did not block the gastrin response to peptone at any time. These results indicate that GR143330X is an effective agent for blocking gastrin-stimulated acid secretion and histamine and somatostatin release in rats. Furthermore, we show for the first time in an intact, in vivo, anesthetized rat model that meal-stimulated activation of gastrin/CCK-B receptors stimulates acid secretion in part by regulating the release of histamine and somatostatin.

Gastric ulceration: the role of thermoxidized palm oil

2016 ◽  
Vol 46 (1) ◽  
pp. 108-119 ◽  
Author(s):  
Agona O Obembe ◽  
Emmanuel O. Ofutet ◽  
Atim B. Antai ◽  
Eme E Osim
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Palm Oil ◽  
Acid Output ◽  
Gastric Ulceration ◽  
Control Group ◽  
Free Access ◽  
Pepsin Secretion ◽  
Content Type

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.

Secretin: a physiological regulator of gastric emptying and acid output in dogs

1994 ◽  
Vol 267 (4) ◽  
pp. G702-G708 ◽  
Author(s):  
H. O. Jin ◽  
K. Y. Lee ◽  
T. M. Chang ◽  
W. Y. Chey ◽  
A. Dubois
Keyword(s):  
Amino Acid ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Dose Range ◽  
Physiological Role ◽  
Plasma Gastrin

Secretin has been known to inhibit gastric acid secretion in several species. However, the physiological role of secretin on the postprandial acid output and gastric emptying in an intact stomach remains controversial. In the present study, we reinvestigated the role of secretin in physiological dose range and endogenous secretin on gastric acid secretion and emptying in the stomach without influencing intragastric luminal pH in dogs. In seven conscious dogs with gastric cannulas, a 4% amino acid meal was administered intragastrically, and three different doses of secretin and an antisecretin serum were infused intravenously in each dog on separate days. Gastric emptying and net acid output were measured using a dye dilution technique, and plasma secretin and gastrin were determined by specific radioimmunoassays. After the meal, gastric emptying was exponential: acid output peaked at 25 min, and plasma concentrations of gastrin and secretin peaked at 15 and 60 min, respectively. Intravenous infusion of secretin at 1.25, 2.5, and 5.0 pmol.kg-1.h-1 dose dependently increased plasma levels of the peptide and suppressed postprandial plasma gastrin response and gastric acid output and emptying of the meal. Immunoneutralization of circulating secretin with a rabbit antisecretin serum abolished the postprandial rise of plasma secretin and significantly increased plasma gastrin, and augmented gastric emptying as well as acid output. It is concluded that, in dogs, secretin plays a physiological role in the regulation of gastric emptying and acid output after a liquid amino acid meal and that these effects may be mediated in part by suppression of the release of gastrin.

scholarly journals Functional Role of Protein Kinase B/Akt in Gastric Acid Secretion

2001 ◽  
Vol 276 (49) ◽  
pp. 46436-46444 ◽  
Author(s):  
Andrea Todisco ◽  
Nonthalee Pausawasdi ◽  
Saravanan Ramamoorthy ◽  
John Del Valle ◽  
Rebecca W. Van Dyke ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Functional Role ◽  
Protein Kinase B

Inhibition of ovine gastric acid secretion by intraduodenal long-chain fatty acids

1982 ◽  
Vol 243 (2) ◽  
pp. G127-G133
Author(s):  
L. M. McLeay ◽  
J. M. Fitzgerald
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Unsaturated Fatty Acids ◽  
Acid Output ◽  
Saturated Fatty Acids ◽  
Fatty Acid Content ◽  
Conscious Sheep

Effects on ovine gastric function of procedures that increase intestinal unsaturated fatty acid content are unknown, and the present aim was to compare the effects of duodenal unsaturated and saturated fatty acids on gastric secretion in conscious sheep. During the maximal gastric secretory response to a meal, 10 ml gallbladder bile alone or with myristic, palmitic, and stearic acids and oleic, linoleic, and linolenic acids were infused into the duodenum at a rate of 5 g fatty acid . h-1 for 1 h. Compared with control 154 mM NaCl (100%), acid output was reduced to 4-7% of control with infusion of oleic, linoleic, and linolenic acids and myristic acids plus bile. Reductions in acid secretion persisted for up to 5 h from the end of infusion. In contrast, the infusion of palmitic and stearic acids with bile caused mean maximal reductions in acid output, respectively, to only 64 and 55% of control, and levels returned to control within 1 h of the end of infusion. Bile infusion alone caused no reduction in acid secretion. Under the conditions used, C18 unsaturated fatty acids and myristic acid were potent inhibitors of ovine gastric acid secretion. The lesser effects of palmitic and stearic acids were probably related to their reduced solubility and absorption.

50 - Reflux Esophagitis after Helicobacter Pylori Eradication: The Role of Gastric Acid Secretion

2018 ◽  
Vol 154 (6) ◽  
pp. S-17
Author(s):  
Francesco Di Mario ◽  
Serena Scida ◽  
Marilisa Franceschi ◽  
Chiara Miraglia ◽  
Kryssia Rodriguez ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Reflux Esophagitis ◽  
Helicobacter Pylori Eradication
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