Neuronal nitric oxide synthase: expression in rat parietal cells

Premaratne, Shyamal; Cheng, Xue; McCarty, John M.; Zaki, Muhammad; McCuen, Robert W.; Johns, Roger A.; Schepp, Wolfgang; Neu, Bruno; Lippman, Robert; Melone, Pamela; Schubert, Mitchell L.

doi:10.1152/ajpgi.2001.280.2.g308

Cited by 20 publications

(11 citation statements)

References 47 publications

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“…Nonetheless, neurons are not the only source of these bioactive molecules. There is also a large amount of nonneuronal 5-HT and NO in the gastric mucosa itself (4,30,31), and we feel that the physiological roles for those molecules in the stomach have not been clearly identified yet. This present report suggests that gastric nonneuronal 5-HT and NO can act in the stomach mucosa as paracrine substances as well after the recognition of nutrients, such as an amino acid like glutamate, in a process similar to the one reported for the duodenal glucose sensing (47).…”

Section: Discussionmentioning

confidence: 94%

Luminal amino acid sensing in the rat gastric mucosa

Uneyama¹,

Niijima²,

Gabriel³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

145

151

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. Luminal amino acid sensing in the rat gastric mucosa. Am J Physiol Gastrointest Liver Physiol 291: G1163-G1170, 2006. First published June 29, 2006 doi:10.1152/ajpgi.00587.2005.-Recent advancements in molecular biology in the field of taste perception in the oral cavity have raised the possibility for ingested nutrients to be "tasted" in the upper gastrointestinal tract. The purpose of this study was to identify the existence of a nutrient-sensing system by the vagus in the rat stomach. Afferent fibers of the gastric branch increased their firing rate solely with the intragastric application of the amino acid glutamate. Other amino acids failed to have the same effect. This response to glutamate was blocked by the depletion of serotonin (5-HT) and inhibition of serotonin receptor 3 (5-HT3) or nitric oxide (NO) synthase enzyme. Luminal perfusion with the local anesthesia lidocaine abolished the glutamate-evoked afferent activation. The afferent response was also mimicked by luminal perfusion with a NO donor, sodium nitroprusside. In addition, the NO donorinduced afferent activation was abolished by 5-HT 3 blockade as well. Altogether, these results strongly suggest the existence of a sensing system for glutamate in the rat gastric mucosa. Thus luminal glutamate would enhance the electrophysiological firing rate of afferent fibers from the vagus nerve of the stomach through the production of mucosal bioactive substances such as NO and 5-HT. Assuming there is a universal coexistence of free glutamate with dietary protein, a glutamate-sensing system in the stomach could contribute to the gastric phase of protein digestion.visceral nutrient sensing; rat vagal gastric afferent; serotonin; nitric oxide THE NUMBER OF ARTICLES DEDICATED to the abdominal vagus nerve that were focused in gut nutrient sensing has increased dramatically over the last decade (33,36,42). This is due to the advancement of techniques that facilitated the study of visceral afferent fibers and their function and characteristic electrophysiological patterns and also due to recognition that these fibers are important for body nutrient homeostasis. Psychophysiological approaches for the understanding of ingestive behavior have demonstrated that the presence of food in the upper gastrointestinal (GI) tract plays a critical role in determining meal size. The vagus nerve is extensively distributed throughout the GI tract, from the posterior region of oral cavity and esophagus to the lowest part of the colon, and functions as the primary neuroanatomical circuit in the gut-brain axis to transmit meal-related signals from the GI mucosa to the central nervous system. This is where regulatory processes (e.g., ingestive behavior, nutrient absorption, GI secretion, and stomach emptying) as well as conscious sensations (e.g., satiety, nausea, and discomfort) take place (5, 22, 37).Recently, it has been shown that taste transduction-related molecules, such as ␣-gustducin and a family of bitter-sensing taste receptors (T 2 Rs), were also expressed at the GI mu...

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Section: Discussionmentioning

confidence: 94%

Luminal amino acid sensing in the rat gastric mucosa

Uneyama¹,

Niijima²,

Gabriel³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

145

151

View full text Add to dashboard Cite

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“…The constitutive form is calcium/calmodulin dependent and implicates the endothelial (eNOS) and neuronal (nNOS) isoform [46]. The expression of nNOS in rat gastric parietal cells was confirmed by Premarante by NADPH-diaphorase histochemistry, nNOS immunostaining, Western blotting and RT-PCR and published in 2001 [47]. However, the technique used for this study differs from our: they used immuno-dissected glands whereas we used hand dissected glands.…”

Section: Discussionmentioning

confidence: 99%

Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats

Kitay

Link

Geibel

2017

Cell Physiol Biochem

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Background/Aims: L-arginine is an important mediator of cell division, wound healing, and immune function. It can be transformed by the nitric oxide synthase (NOS) to nitric oxide (NO), an important cell signaling molecule. Recent studies from our laboratory demonstrate specific effects of L-arginine (10mM) exposure on gastric acid secretion in rat parietal cells. Methods: Studies were performed with isolated gastric glands and the pH sensitive dye BCECF-AM +/- L-arginine to examine its effects on acid secretion. The direct NO-donor diethylamine NONOate sodium salt hydrate, was also used while monitoring intracellular pH. The specific inhibitor of the intracellular NO signal cascade ODQ was also used. Results: We found that gastric proton extrusion was activated with application of L-arginine (10mM), in a separate series when L-arginine (10mM) + L-NAME (30µM) were added there was no acid secretion. Addition of the NO-donor diethylamine NONOate sodium salt hydrate (10µM) also induced acid secretion. When the selective sGC-inhibitor ODQ was added with NONOate we did not observe acid secretion. Conclusion: We conclude that L-arginine is a novel secretagogue, which can mediate gastric acid secretion. Furthermore, the intake of L-arginine causes direct activation of the H⁺, K⁺ ATPase and increased proton extrusion from parietal cells resulting in the increased risk for acid-related diseases. The NO/sGC/cGMP pathway has never been described as a possible intracellular mechanism for H⁺, K⁺ ATPase activation before and presents a completely new scientific finding. Moreover, our studies demonstrate a novel role for L-NAME to effectively eliminate NOS induced acid secretion and thereby reducing the risk for L-arginine inducible ulcer disease.

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“…On the basis of studies on chloride secretion and changes in short-circuit current in the isolated rat distal colon, King et al (2004) suggested that NO is a secretomotor neurotransmitter in response to serotonin. Expression of nNOS in parietal cells suggests a participation of endogenous NO in the regulation of gastric acid secretion (Premaratne et al, 2001). Helicobacter pylori increased pepsinogen secretion from dispersed human peptic cells through a Ca 2ϩ -and NO-mediated intracellular pathway (Lorente et al, 2002).…”

Section: Secretion and Neurogenic Nitric Oxidementioning

confidence: 99%