Acid Production

Acid Production

Organs – Stomach

Furthermore, they suggest that EOCZ has potential therapeutic application for the treatment of gastric ulcers. [6] [7][8].

acid secretion in the stomach is controlled by

Furthermore potentiating interactions occur between histamine, gastrin, and cholinergic agents which may account for the interdependence of secretagogue action observed in vivo. Direct potentiating interactions occur between histamine and gastrin and histamine and carbachol but not between carbachol and gastrin. However, in the presence of histamine, carbachol, and gastrin, a three-way potentiation does occur. By interfering with the potentiating interactions between stimulants, anticholinergic agents and cimetidine display an apparent cross-specificity in vitro that resembles the effects of these agents in intact mucosa.

Highly purified (85%) ECL cells were collected from rat stomach using repeated counter-flow elutriation and cultured for 48 h before experiments were conducted.

These findings were corroborated by immunohistochemical detection of TAS2R10 and transducin in different gastric cell types for which useful antisera were available. So far, to our knowledge, only one validated antibody against human TAS2R38 (38) is known. Neither caffeine nor HED bind to TAS2R38.

Secondly, to evaluate the effects of endogenous and exogenous H 2 S on eNOS gene expression, the mRNA level of eNOS was measured by semiquantitative real-time PCR. As shown in Figure 4(a), gene expression of eNOS in PAG-treated rats was significantly lower than in control rats. This level in NaHS- and L-cysteine-treated rats was significantly increased as compared with the corresponding control rats (Figures 4(a) and 4(b)). These findings show that endogenous and exogenous H 2 S stimulate eNOS mRNA expression.

Exclusion of Off-Target Effects Using Whole-Genome Sequencing.

These data demonstrate that TAS2R43 is involved in caffeine’s action on proton secretion in HGT-1 cells. The gastric phase is mediated by the vagus nerve and by the release of gastrin. The acidity of the gastric contents after a meal is buffered by proteins so that overall it remains around pH3 (acidic) for approximately 90 minutes.

The enteroendocrine cells also secrete glucose -dependent insulinotropic peptide. Originally called gastric-inhibitory peptide, it is no longer thought to have a significant effect on the stomach. Rather, it probably stimulates insulin secretion in preparation for processing the nutrients that are about to be absorbed by the small intestine. Stretching of the duodenum (the first segment of the small intestine ) enhances gastric function via the vagal nerve, as the chyme causes the secretion of gastrin, which stimulates the stomach. Control of secretion from rat stomach ECL cells in situ and in primary culture.

How Inflammation Causes Gastric Cancer

The inhibition of histamine-induced secretion makes it unlikely that these effects of FPL 52694 are due to prevention of endogenous histamine release. N-(3-[3-(1-Piperidinylmethyl)phenoxy]propyl)-acetoxyacetamide++ + hydrochloride (TZU-0460) was compared with cimetidine for the effects on gastric acid secretion in dog and rat and on ulcer formation in rat. TZU-0460 as well as cimetidine, given i.v.

acid secretion in the stomach is controlled by

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