Nitric oxide generators and cGMP stimulate mucus secretion by rat gastric mucosal cells

Brown, James F.; Keates, Andrew C.; Hanson, Peter J.; Whittle, B. J. R.

doi:10.1152/ajpgi.1993.265.3.g418

Cited by 141 publications

(142 citation statements)

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“…Within the gastrointestinal tract, NO protects the stomach epithelium by stimulating mucosal and bicarbonate secretions [4,20,21]. NO may also confer protection to the mucosal layer by inhibiting gastric acid secretion and leukocyte adhesion to the epithelium [4,5,22,23].…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Sensors for Biological Applications

2018

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Nitric oxide (NO) is an essential signaling molecule within biological systems and is believed to be involved in numerous diseases. As a result of NO's high reaction rate, the detection of the concentration of NO, let alone the presence or absence of the molecule, is extremely difficult. Researchers have developed multiple assays and probes in an attempt to quantify NO within biological solutions, each of which has advantages and disadvantages. This review highlights many of the current NO sensors, from those that are commercially available to the newest sensors being optimized in research labs, to assist in the understanding and utilization of NO sensors in biological fields.

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Section: Introductionmentioning

confidence: 99%

Nitric Oxide Sensors for Biological Applications

2018

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“…mucosal blood flow (Pique et al, 1989), protection of gastric (MacNaughton et al, 1989) and intestinal ) mucosa, gastric mucus secretion (Brown et al, 1993) and intestinal electrolyte and fluid transport.…”

Section: Introductionmentioning

confidence: 99%

Significance of nitric oxide in the stimulation of intestinal fluid absorption in the rat jejunum in vivo

Schirgi‐Degen

Beubler

1995

British J Pharmacology

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1 The effects of inhibiting nitric oxide (NO)-synthase on fluid transport, mucosal cyclic GMP and cyclic AMP levels and intraluminal prostaglandin E2 (PGE2)-release were studied in a model of ligated jejunal loops of anaesthetized rats in vivo. Experiments were performed under basal conditions as well as under conditions, when net fluid secretion was induced by Escherichia coli heat stable enterotoxin a (E. coli STa) or PGE2. 2 Intravenous infusion of the NO-synthase inhibitor N0-nitro-L-arginine methyl ester (L-NAME, 0.25-50mgrkg-', 45min) dose-dependently reversed net fluid absorption to net secretion, whereas infusion of D-NAME, the inactive enantiomer of L-NAME, in corresponding doses did not influence net fluid transport. Nw-nitro-L-arginine (L-NOARG, 25 mg kg-'), another NO-synthase inhibitor, also elicited net secretion of fluid. -3 L-NAME (25 mg kg ')-induced net fluid secretion was reversed to net absorption by infusion of L-arginine (400 mg kg') or sodium nitroprusside (1 mg kg-') and s.c. administration of indomethacin (10 mg kg-'). Hexamethonium (1 mg kg-', s.c.), a ganglionic blocker and granisetron (100 gsg kg-', s.c.), a 5-HT3-receptor antagonist, did not influence L-NAME-induced net secretion. 4 Net fluid secretion induced by intraluminal instillation of E. coli STa (10 units ml-') was enhanced by infusion of L-NAME (25mgkg-') and was inhibited by infusion of L-arginine (400mgkg-') and sodium nitroprusside (1 mg kg-'). D-Arginine (400 mg kg-') did not influence E. coli STa-induced fluid secretion. Likewise, net fluid secretion induced by i.a. infusion of PGE2 (79 ng ml-, 30 min) was enhanced by infusion of L-NAME and was inhibited by L-arginine and sodium nitroprusside. D-Arginine (400 mg kg-') did not influence PGE2-induced fluid secretion. 5 PGE2 levels in intraluminal fluid were not elevated after infusion of L-NAME (25mgkg-') compared to controls. 6 Mucosal cyclic GMP and cyclic AMP levels after L-NAME-treatment were not different from control values. 7 These results indicate that nitric oxide plays an important role in the regulation of intestinal fluid transport. The data suggest a nitric oxide-dependent proabsorptive tone in the intestine, which possibly involves the enteric nervous system and suppression of prostaglandin formation. This proabsorptive tone also may downregulate fluid secretion induced by E. coli STa or PGE2.

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“…Of particular importance with regard to chemopreventive therapy are its effects on the gastrointestinal tract. The release of NO might compensate for NSAID-induced reductions in prostaglandin levels through the capacity of NO to increase mucosal blood circulation (12) and mucous release (13), and NO's properties of inhibiting neutrophil adherence and activation (14,15). Notably, NO-NSAIDs are associated with a significant reduction in renal toxicity as well (16,17).…”

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confidence: 99%

Modulation of Carcinogen Metabolism by Nitric Oxide-Aspirin 2 Is Associated with Suppression of DNA Damage and DNA Adduct Formation

MacDonald¹,

Cheng²,

Roberts³

et al. 2009

Journal of Biological Chemistry

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Accumulating evidence suggests that non-steroidal anti-inflammatory drugs (NSAIDs) 2 decrease the risk of developing premalignant lesions and several types of cancer (1, 2). The potential for NSAIDs to serve as chemoprotective agents has been particularly evident for colorectal cancer, as demonstrated by epidemiological and clinical studies, as well experimental animal models. Unfortunately, even at low doses, long term NSAID usage is associated with significant gastrointestinal and renal side-effects, some of which are potentially lifethreatening (3, 4). In fact, in 1998, the number of deaths in the United States from NSAID complications paralleled the number of deaths from AIDS (5, 6). This has prompted the emergence of novel strategies in efforts to maintain the desired pharmacological effects of NSAIDs, while diminishing the deleterious properties. One such strategy led to the development of coxibs, selective cyclooxygenase 2 inhibitors, which, although they do in fact reduce gastrointestinal complications, are also associated with increased cardiovascular side-effects (7-9). Recent development of nitric oxide (NO)-donating NSAIDs (10) has refueled interest in utilizing this class of drugs in chemoprevention. NO-NSAIDs consist of a NO-releasing moiety covalently bound to a spacer (via ester linkage), which in turn is bound to the parent NSAID (Fig. 1). NO is recognized as a key modulator in a wide array of physiological pathways (11). Of particular importance with regard to chemopreventive therapy are its effects on the gastrointestinal tract. The release of NO might compensate for NSAID-induced reductions in prostaglandin levels through the capacity of NO to increase mucosal blood circulation (12) and mucous release (13), and NO's properties of inhibiting neutrophil adherence and activation (14,15). Notably, NO-NSAIDs are associated with a significant reduction in renal toxicity as well (16,17).Current evidence shows that NO-NSAIDs are substantially superior compared with their NSAID counterparts with respect to a number of biological end points, including the induction of apoptosis (18 -20), and inhibition of cellular proliferation (18,20,21), with NO-aspirin having the most potent effects (10). Studies indicate that not only are both the NSAID and the NO moieties responsible for the physiological manifestations of the drugs (22), but, particularly in the case with NO-

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Nitric oxide generators and cGMP stimulate mucus secretion by rat gastric mucosal cells

Cited by 141 publications

References 0 publications

Nitric Oxide Sensors for Biological Applications

Nitric Oxide Sensors for Biological Applications

Significance of nitric oxide in the stimulation of intestinal fluid absorption in the rat jejunum in vivo

Modulation of Carcinogen Metabolism by Nitric Oxide-Aspirin 2 Is Associated with Suppression of DNA Damage and DNA Adduct Formation

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