Gastric acid secretion

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The results of the present study clearly showed that an increase in NO concentration and prostaglandins release resulted from the administration of NaHS inhibited and neutralize the gastric acid output. The findings also suggest that H 2 S exerts both an antisecretory effect by reducing the acid output as shown by the present work and at the same time an antacid activity by inducing bicarbonate production as shown by the previous reports [11]. After the surgical preparation, basal gastric acid secretion was allowed to stabilize for at least 30 min. At the end of this period, mean acidity of two first 15 min of gastric effluent considered as basal acid output.

It is also plausible that NO can exert its effect alone, without acting through other signalling molecules. Under experimental conditions, NO can induce nitrosylation and nitration of cellular proteins, although that is probably not the case in vivo, since those two processes often result permanent damage to vital functions [30].

Quantity and quality were checked spectrophotometrically. Reverse transcription was carried out with 2 µg RNA and the High Capacity cDNA Reverse Transcription Kit (Thermo Fisher Scientific). Real-time PCR was performed with an Applied Biosystems StepOneplus Real Time PCR system and Fast SYBR Green Master Mix (Thermo Fisher Scientific).

pylori infection but still the cases of idiopathic ulcers are increasing. Therefore, a combination of pharmacological and endoscopic approaches is used for the management of ulcers. exchangers, which are also expressed in the parietal cell, may function to maintain pH homeostasis (8) rather than playing a direct role in support of acid secretion.

Vasoactive intestinal peptide, cholecystokinin, and secretin all inhibit production. Since it is known that guanylate cyclase is a general target of NO in many cell systems, some investigators have suggested that NO exerts its effects via cyclic guanosine 3′,5′-monophosphate (cGMP) in both rat and rabbit parietal cells [13, 15]. An ongoing study in our laboratory will show whether this is the case in human parietal cells. Downstream effects of cGMP may include activation of a number of effectors, such as ion channels, protein kinases, and phosphodiesterases [29].

Ample data from clinical trials and observational experience have confirmed the utility of these agents in the treatment of acid peptic diseases, with differential efficacy and safety characteristics between and within drug classes. Paradigms in their speed and duration of action have underscored the need for new chemical entities that, from a single dose, would provide reliable duration of acid control, particularly at night.

The mRNA expression of H + /K + -ATPase α-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 H 2 S. These three chemical stimuli converging on the parietal cells have syndergistic effects on stomach acid production. This means that substantially more stomach acid is secreted by parietal cells when stimulated by all three molecules simultaneously.

This phase continues until the food has left the stomach. Gastrin is in the stomach and stimulates the gastric glands to secrete pepsinogen (an inactive form of the enzyme pepsin) and hydrochloric acid. The secretion of gastrin is stimulated by food arriving in the stomach.

The numbers of antral gastrin cells were doubled and the numbers of antral somatostatin cells half that in the controls. These results show that long-standing lansoprazole-evoked hypergastrinemia affects the ECL cell similarly to omeprazole, ranitidine and other acid secretion inhibitors. To further understand the role of the peptide hormone gastrin in the development and function of the stomach, we have generated gastrin-deficient mice by gene targeting in embryonic stem cells. Mutant mice were viable and fertile, without obvious visible abnormalities.

We studied the effects of NO on acid secretion induced by various stimulants in gastric glands isolated from stomach biopsies from human. Morphological examination of the hematoxylin-eosin-stained slides revealed that the isolation procedure had successfully yielded whole-gland preparations and that parietal cells were present in the gastric glands. Immunohistochemical analysis showed that the isolated glands contained eNOS-immunoreactive cells (Fig. 1), which agrees with results obtained using other types of mucosal preparations [22]. Control experiments were primary antibody was excluded showed no immunoreactivity. Our results show that NO inhibits gastric acid secretion in isolated human gastric glands, and that there is endogenous formation of NO within the glandular epithelium in the vicinity of the parietal cells.

Here, we show that caffeine increased cAMP levels in HGT-1 cells, an effect that was inhibited by HED. HED itself reduced the cAMP level in HGT-1 cells, but did not affect proton secretion in HGT-1 cells. Therefore, it remains unclear whether or which signaling pathways are affected by HED.

These findings together show that exogenous and endogenous H 2 S increase the prostaglandins production/release. Therefore, due to the antisecretory and acid-neutralizing properties of PGs, it could conclude that a reduction of the acid output/an increase in gastric pH by NaHS in response to distention is partly mediated through an increase in the PGs production. (2015 ) Identification of catechin, syringic acid, and procyanidin b2 in wine as stimulants of gastric acid secretion .

The dual delayed-release PPI dexlansoprazole seems to respond for some of the limitations other PPIs have. discussed below, the data suggest that a more important factor may be impaired development of parietal cells. mechanisms must also maintain the appropriate electrical and ionic driving forces that are required for acid secretion. gastric mucosa (Table II), consistent with the possibility that both exchangers contribute to the maintenance of parietal cell volume.

acid secretion in the stomach is controlled by

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