Nitric oxide stimulates prostaglandin synthesis in cultured rabbit gastric cells

Uno, Hironori; Fukuda, Takashi; Yu, Hidenori; Fujiwara, Yasuhiro; Higuchi, Kazuhide; Inoue, Masayasu; Kobayashi, Kenzo

doi:10.1016/s0090-6980(97)00013-0

Cited by 26 publications

(20 citation statements)

References 28 publications

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“…Salvemini et al also reported that NO directly interacted with COX to cause an increase in the enzymatic activity (14). In addition, Uno et al also reported that NO stimulated prostaglandin synthesis in cultured rabbit gastric cells (11). These reports are consistent with our results, although the experimental conditions were different from each other.…”

Section: Discussionsupporting

confidence: 91%

“…Recently, Uno et al reported that NO stimulated syntheses of PGs, such as PGE 2 and PGI2, in cultured rabbit gastric cells (11). These PGs have been known to inhibit gastric lesions in rats.…”

Section: Discussionmentioning

confidence: 99%

“…Uno et al reported that NO stimulated syntheses of PGs, such as PGE2 and PGI2, in cultured rabbit gastric cells (11). Whittle et al also reported that endogenous NO formed from L-arginine, acting in concert with PGI 2 and sensory neuropeptides, had a role in modulation of gastric mucosal integrity in anesthetized rats (13).…”

mentioning

confidence: 99%

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Nitric Oxide Donating Compounds Inhibit HCl-Induced Gastric Mucosal Lesions Mainly via Prostaglandin

Uchida

Matsueda

Shoda

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-Prostaglandin (PG) and nitric oxide (NO) have been known to inhibit the lesion formation induced by necrotic agents. However, no clear correlation between PG and NO has been shown in the gastroprotective action against necrotic agent-induced gastric mucosal lesions in rats. Thus, the present study was performed to clarify this correlation. Gastric mucosal lesions were induced by the oral administration of 0.6 M HCl in rats. 16,16-Dimethyl PGE2 (0.3 -3 mg/ kg, p.o.; dim-PGE2), sodium nitrite (0.3 and 1 mg /kg, s.c.) and sodium nitroprusside (30 and 100 m g/kg, i.v.; SNP) dose-dependently inhibited the lesion formation. Orally administered sodium nitrite or SNP (3 mg/kg) also significantly inhibited the lesion formation. The gastroprotective action by dim-PGE 2 was not affected by the pre-treatment with N G -nitro-Larginine methylester (10 mg /kg, i.v.). The gastroprotective effect by sodium nitrite or SNP was markedly attenuated by the pre-treatment with indomethacin (10 mg/ kg, s.c.). These findings suggest that NO donating compounds inhibit the HCl-induced mucosal lesions mainly through prostaglandin, but dim-PGE2 directly inhibits the lesions without involvement of NO in rats.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Nitric Oxide Donating Compounds Inhibit HCl-Induced Gastric Mucosal Lesions Mainly via Prostaglandin

Uchida

Matsueda

Shoda

et al. 2001

Japanese Journal of Pharmacology

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“…An effective inhibition of NOS was apparent by the rise in systemic blood pressure and mucosal vascular resistance seen after intravenous administration of the drug. NO has been shown to stimulate PG synthesis in the gastric mucosa (39), which could suggest that the nitritemediated effects are ultimately mediated by PGs. This also seems unlikely since in the experiments with indomethacin the mucosal blood flow response to nitrite was unaffected.…”

Section: Discussionmentioning

confidence: 99%

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Björne¹,

Petersson²,

Phillipson³

et al. 2004

J. Clin. Invest.

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Salivary nitrate from dietary or endogenous sources is reduced to nitrite by oral bacteria. In the acidic stomach, nitrite is further reduced to NO and related compounds, which have potential biological activity. We used an in vivo rat model as a bioassay to test effects of human saliva on gastric mucosal blood flow and mucus thickness. Gastric mucosal blood flow and mucus thickness were measured after topical administration of human saliva in HCl. The saliva was collected either after fasting (low in nitrite) or after ingestion of sodium nitrate (high in nitrite). In additional experiments, saliva was exchanged for sodium nitrite at different doses. Mucosal blood flow was increased after luminal application of nitrite-rich saliva, whereas fasting saliva had no effects. Also, mucus thickness increased in response to nitrite-rich saliva. The effects of nitrite-rich saliva were similar to those of topically applied sodium nitrite. Nitrite-mediated effects were associated with generation of NO and S-nitrosothiols. In addition, pretreatment with an inhibitor of guanylyl cyclase markedly inhibited nitrite-mediated effects on blood flow. We conclude that nitrite-containing human saliva given luminally increases gastric mucosal blood flow and mucus thickness in the rat. These effects are likely mediated through nonenzymatic generation of NO via activation of guanylyl cyclase. This supports a gastroprotective role of salivary nitrate/nitrite.

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“…Thus, it is also possible that mucosal acidification increases NO release through the stimulation of capsaicin-sensitive sensory neurons. On the other hand, several studies have reported that NO or NO donors stimulate PG production in various organs and cells (8,35,36). Uno et al (35) reported that the NO donor S-nitroso-N-acetyl penicillamine stimulates PGE 2 production in rat gastric epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Distinct mechanisms of acid-induced HCO₃⁻secretion in normal and slightly permeable stomachs

Aihara

Sasaki²,

Ise³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Distinct mechanisms of acidinduced HCO 3 Ϫ secretion in normal and slightly permeable stomachs. Am J Physiol Gastrointest Liver Physiol 291: G464 -G471, 2006. First published May 18, 2006 doi:10.1152/ajpgi.00048.2006.-We investigated the regulatory mechanism of acid-induced HCO 3 Ϫ secretion in the slightly permeable rat stomach after an exposure to hyperosmolar NaCl. Under urethane anesthesia, a rat stomach was mounted on a chamber and perfused with saline, and the secretion of HCO 3 Ϫ was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Acidification of the normal stomach with 100 mM HCl increased HCO 3 Ϫ secretion, and this response was totally inhibited by pretreatment with indomethacin but not N G -nitro-L-arginine methyl ester (L-NAME) or chemical ablation of capsaicin-sensitive afferent neurons. Exposure of the stomach to 0.5 M NaCl deranged the unstirred mucus gel layer without damaging the surface epithelial cells. The stomach responded to 0.5 M NaCl by secreting slightly more HCO 3 Ϫ , in an indomethacin-inhibitable manner, and responded to even 10 mM HCl with a marked rise in HCO 3 Ϫ secretion, although 10 mM HCl did not have an effect in the normal stomach. The acid-induced HCO 3 Ϫ response in the NaCl-treated stomach was significantly but partially attenuated by indomethacin, L-NAME, or sensory deafferentation and was totally abolished when these treatments were combined. These results suggest that gastric HCO 3 Ϫ secretion in response to acid is regulated by two independent mechanisms, one mediated by prostaglandins (PGs) and the other by sensory neurons and nitric oxide (NO). The acid-induced HCO 3 Ϫ secretion in the normal stomach is totally mediated by endogenous PGs, but, when the stomach is made slightly permeable to acid, the response is markedly facilitated by sensory neurons and NO.gastric HCO 3 Ϫ secretion; mucosal acidification; capsaicin-sensitive afferent neurons; prostaglandin; nitric oxide; rat THE SECRETION of HCO 3 Ϫ plays a crucial role in the protection of the gastroduodenal mucosa from acid (5, 10). The secretion increases in response to mucosal acidification, and the process is mediated by multiple factors, including endogenous prostaglandins (PGs) and nitric oxide (NO) as well as neuronal pathways (12,22,29,30). Recently, we found that the mechanism underlying acid-induced HCO 3 Ϫ secretion in the stomach differed depending on the concentration of acid; the response caused by 100 mM HCl was mediated only by PGs, whereas that caused by 200 mM HCl was mediated by both capsaicinsensitive afferent neurons and NO in addition to PGs (1). It is assumed that 100 mM HCl applied topically to the stomach increases PG biosynthesis by itself but does not acidify the mucosa enough to activate afferent neurons, resulting in an increase of HCO 3 Ϫ secretion that is totally dependent on endogenous PGs but not afferent neurons or NO.Mucus adherent to the luminal surface of the mucosa provides a zone of low turbulence (unstirred layer), allowing the development of a gradient f...

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Nitric oxide stimulates prostaglandin synthesis in cultured rabbit gastric cells

Cited by 26 publications

References 28 publications

Nitric Oxide Donating Compounds Inhibit HCl-Induced Gastric Mucosal Lesions Mainly via Prostaglandin

Nitric Oxide Donating Compounds Inhibit HCl-Induced Gastric Mucosal Lesions Mainly via Prostaglandin

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Distinct mechanisms of acid-induced HCO₃⁻secretion in normal and slightly permeable stomachs

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Nitric oxide stimulates prostaglandin synthesis in cultured rabbit gastric cells

Cited by 26 publications

References 28 publications

Nitric Oxide Donating Compounds Inhibit HCl-Induced Gastric Mucosal Lesions Mainly via Prostaglandin

Nitric Oxide Donating Compounds Inhibit HCl-Induced Gastric Mucosal Lesions Mainly via Prostaglandin

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Distinct mechanisms of acid-induced HCO3−secretion in normal and slightly permeable stomachs

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Distinct mechanisms of acid-induced HCO₃⁻secretion in normal and slightly permeable stomachs