Gastric acid

At visits 9-11, three new subjects joined to replace dropouts. There, an empty gelatin capsule (Coni-Snap size 1; Capsugel), 150 mg caffeine encapsulated, or 150 mg caffeine encapsulated with 30 mg HED were administered with 125 mL water 25 min before the alkaline solution. For exclusive activation of TAS2Rs in the mouth (delivery protocol 3), the subjects swallowed 125 mL water and rinsed their mouth with 150 mg caffeine diluted in 125 mL water without swallowing the caffeine 5 min after swallowing the alkaline solution. Reacidification time (i.e., time until original pH is reached again after administration of the alkaline challenge) as well as the slope of the gastrogram were analyzed by using Heidelberg Detection System software and ImageJ software (National Institutes of Health). Delta reacidification time was calculated by substraction of the reacidification time of the water or empty capsule control from the reacidification time after the treatment.

Gastric Secretory Products

Unlike acetylcholine, the neuropeptides pituitary adenylate cyclase-activating peptide and vasoactive intestinal peptide mobilize ECL-cell histamine. Whether vagally stimulated acid secretion reflects an effect of the enteric nervous system on the ECL cells (neuropeptides) and/or a direct one on the parietal cells needs to be further investigated. In an earlier study, we found morphological support that endogenous NO plays a role in regulation of parietal cell function [22]. Also, the

and wild-type mice were measured at 18 days, 9 weeks, and 6 months of age as described previously (14). Mice were euthanized 15 min after subcutaneous injection of histamine (2 μg/g body weight) and the intact stomach was removed. Although the plasma half-lives of PPIs are quite short, their mechanism of action enables most patients to be satisfactorily treated with once-daily dosing. Generally it does not matter whether the dose is given in the morning or the evening.

ATPase. This channel uses ATP energy to exchange potassium ions in the stomach with hydrogen ions in the parietal cell. This article will outline the production of stomach acid, the regulation of this and some clinical conditions that result from this process going wrong. Gastric inhibitory peptide (GIP) is in the duodenum and decreases stomach churning in order to slow the emptying of the stomach.

Blots were hybridized with probes to gastrin, gastric H + ,K + -ATPase α- and β-subunits, AE2, NHE2, pepsinogen, intrinsic factor, and the L32 ribosomal protein subunit (as a loading control). This newer class of drugs includes omeprazole, lansoprazole and pantoprazole. All these drugs substantially inhibit acid secretion. Their chemical structures differ only minimally, and for practical purposes their pharmacology is identical. When acid secretion is stimulated with histamine, the systemic adverse effects of histamine can be prevented by a conventional antihistamine drug without affecting acid secretion.

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

Furthermore, AG-1749 prevented gastric lesions induced by absolute ethanol or acidified aspirin, and accelerated the healing of acetic acid-induced gastric or duodenal ulcers in rats. The inhibitory potency of AG-1749 in dogs was much the same as that of omeprazole and about half that of ranitidine. However, it was about 2 to 10 times more potent than omeprazole and 4 to 34 times more potent than ranitidine in rats.

In conclusion the present study showed the following. (i) Administration of NaHS, a H 2 S donor, and L-cysteine, H 2 S precursor, reduced the acid output in response to gastric distention. (ii) Pretreatment with L-NAME mitigated the inhibitory effect of NaHS on distention-induced gastric acid secretion. (iii) The mRNA level of eNOS and COX-2 was significantly increased by NaHS and L-cysteine.

Although there is little known about human ECL-cells and the effects of NO on histamine-release there are studies that indicate species differences in other histamine-secreting cells. For example, rat mast cells have been shown to produce an “NO-like factor” which inhibits histamine-release [32] while there are investigations that indicate that NO does not affect histamine-secretion in human basophils [33]. At present we can only establish differences in inhibitory response to l-arginine for histamine and db-cAMP stimulation.

Omeprazole, infused into the Heidenhain pouch, caused a dose-dependent inhibition of the Heidenhain pouch response to intravenous histamine without any significant change in the acid response of the main stomach and plasma concentrations of the drug. This indicates that omeprazole may exhibit local inhibitory action on the oxyntic glands. Omeprazole did not affect gastric mucosal integrity or the rate of alkaline secretion from the gastroduodenal mucosa or the pancreas stimulated by duodenal acidification or secretin. The effects of the mast-cell stabilizing agent, FPL 52694, on gastric acid secretion in conscious dogs with gastric fistulae have been studied. FPL 52694 (5 or 10 mg kg-1 h-1) given intravenously during a plateau response to pentagastrin stimulation (2 micrograms kg-1 h-1) caused a maximum inhibition of acid output of about 50% but had no significant effect on volume output so that the [H+] in the

cells exhibited an expansion of the secretory canaliculi and appeared to be secreting acid at high rates (14). Thus, NHE2 is essential for parietal cell survival but does not appear to be directly involved in gastric acid secretion. Safe and effective inhibition of gastric acid secretion has been a long-desired goal of clinicians who treat acid-related diseases such as gastro-oesophageal reflux disease and peptic ulcer. Nowadays, two classes of drug – the histamine H 2 -receptor antagonists and the proton pump inhibitors (PPI) – achieve this goal with a high level of success.

The presence of chyme within the duodenum also stimulates entero-endocrine cells to release cholecystokinin and secretin, both of which play a variety of important roles in completing digestion, but also inhibit gastric acid secretion. Finally, enterochromaffin like cells in the stomach secrete histamine which binds to H2 receptors on the parietal cells. These cells release histamine in response to the presence of gastrin and ACh. This leads to increased fusion however it is via the secondary messenger cAMP as opposed to calcium in the other methods.

In a previous study conducted by our research group [22], examination of the glandular epithelium of specimens of human oxyntic mucosa revealed that one particular type of cells contained NOS. These eNOS-immunoreactive cells, defined as endocrine cells, were in close contact with parietal cells. These two characteristics suggest that cells of this type release NO, which thus might be a paracrine regulator that directly affects the function of parietal cells.

Acid secretion was stimulated after intravenous injection of PACAP into rats treated with somatostatin antibody. PACAP is a candidate as a mediator of neural regulation of acid secretion. Histamine H2-receptor antagonists and proton pump inhibitors are the main classes of drug used to inhibit gastric acid secretion.

According to Figure 4, eNOS mRNA expression increased in L-NAME + NaHS-treated animals rats as compared with the control rats while the luminal release of NO and also gastric acid output did not change compared with the control group. These results show that NaHS upregulated the gene expression of eNOS like NaHS-treated group but it did not affect the enzyme activity and NO production/release as well as the gastric acid output because of the presence of L-NAME. -nitro-L-arginine methyl ester, L-NAME (10 mg/kg, i.v.), 5 min before the administration of NaHS (80 μg/kg, i.v.) [11].

acid secretion in the stomach is controlled by

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