scholarly journals Nitric Oxide Released from Luminal S-Nitroso-N-Acetylcysteine Increases Gastric Mucosal Blood Flow

Molecules ◽  
2015 ◽  
Vol 20 (3) ◽  
pp. 4109-4123 ◽  
Author(s):  
Gabriela de Souza ◽  
Patricia Taladriz-Blanco ◽  
Lício Velloso ◽  
Marcelo de Oliveira
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow

Cholecystokinin secretagogue-induced gastroprotection: role of nitric oxide and blood flow

2003 ◽  
Vol 284 (3) ◽  
pp. G399-G410 ◽  
Author(s):  
Sonlee D. West ◽  
Kenneth S. Helmer ◽  
Lily K. Chang ◽  
Yan Cui ◽  
George H. Greeley ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Gastric Injury ◽  
Protective Mechanism ◽  
Adaptive Cytoprotection ◽  
Mucosal Defense ◽  
Calcium Dependent

This study was done to examine the role of CCK in gastric mucosal defense and to assess the gastroprotective roles of nitric oxide and blood flow. In rats, the CCK secretagogues oleate and soybean trypsin inhibitor augmented gastric mucosal blood flow and prevented gastric injury from luminal irritants. Type A CCK receptor blockade negated CCK secretagogue-induced gastroprotection and exacerbated gastric injury from bile and ethanol but did not block adaptive cytoprotection. CCK secretagogue-induced gastroprotection and hyperemia were negated by nonselective nitric oxide synthase (NOS) inhibition ( N G-nitro-l-arginine methyl ester) but not by selective inducible NOS inhibition (aminoguanidine). Gastric mucosal calcium-dependent NOS activity, but not calcium-independent NOS activity, was increased following CCK and CCK secretagogues. The release of endogenous CCK plays a role in the intrinsic gastric mucosal defense system against injury from luminal irritants. The protective mechanism appears to involve increased production of nitric oxide from primarily the constitutive isoforms of NOS and a resultant increase in blood flow.

Gastric mucosal blood flow response to stress in streptozotocin diabetic rats: Regulatory role of nitric oxide

1997 ◽  
Vol 32 (6) ◽  
pp. 726-733 ◽  
Author(s):  
Hitoshi Suzuki ◽  
Tooru Shimosegawa ◽  
Akihiko Satoh ◽  
Kenji Kimura ◽  
Shuichi Ohara ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Diabetic Rats ◽  
Blood Flow Response ◽  
Flow Response ◽  
Response To Stress ◽  
Streptozotocin Diabetic Rats

Renal failure increases gastric mucosal blood flow and acid secretion in rats: role of endothelium-derived nitric oxide

1992 ◽  
Vol 263 (1) ◽  
pp. G75-G80 ◽  
Author(s):  
E. Quintero ◽  
P. H. Guth
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Chronic Renal Failure ◽  
Acid Secretion ◽  
Acid Output ◽  
Muscle Blood Flow ◽  
Specific Inhibitor ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow

Because of the contradictory findings in clinical studies, and the complete lack of animal studies, the purpose of this investigation was to characterize the changes in gastric mucosal blood flow (GMBF) and acid secretion in an animal model of chronic renal failure. Rats with chronic renal failure induced by partial kidney infarction had a significantly higher basal GMBF and lower gastric vascular resistance than control rats. The gastric acid secretory and mucosal hyperemic response to pentagastrin were markedly enhanced in renal failure rats. Because endothelial-derived nitric oxide (NO) is an endogenous vasodilator that regulates gastric vascular tone, we hypothesized that NO mediates the gastric hyperemia of renal failure rats. The administration of N omega-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of NO formation, produced a significantly greater decrease in GMBF in renal failure rats than in control rats, including a low dose inhibiting the basal hyperemia in renal failure rats but having no effect in control rats. It also attenuated pentagastrin-stimulated GMBF in both groups. In contrast, L-NAME produced a similar decrease in basal skeletal muscle blood flow in both renal failure and control rats. We conclude that in the renal failure rat 1) there is an increased basal GMBF and pentagastrin-stimulated acid output and GMBF, and 2) this gastric mucosal hyperemia is mediated by NO.

Peripheral mediators involved in gastric hyperemia to vagal activation by central TRH analog in rats

1998 ◽  
Vol 274 (1) ◽  
pp. G170-G177 ◽  
Author(s):  
Ágnes Király ◽  
Gábor Sütö ◽  
Paul H. Guth ◽  
Yvette Taché
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Gastric Acid ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Hydrogen Gas ◽  
Hydrogen Gas Clearance ◽  
Afferent Fibers ◽  
Intracisternal Injection

Mechanisms mediating the increase in gastric mucosal blood flow (GMBF) induced by the stable thyrotropin-releasing hormone (TRH) analog RX-77368 injected intracisternally at a gastric acid secretory dose (30 ng) were investigated using hydrogen gas clearance in urethan-anesthetized rats. The histamine H1 receptor antagonist pyrilamine (intravenously), capsaicin (subcutaneously, −10 days), and N G-nitro-l-arginine methyl ester (l-NAME, intracisternally) failed to impair the 150% rise in GMBF induced by intracisternal injection of RX-77368. By contrast, atropine (subcutaneously) and N G-monomethyl-l-arginine (intravenously) completely inhibited the increase in GMBF evoked by intracisternal RX-77368. l-NAME (intravenously) blocked the intracisternal RX-77368-induced increase in GMBF in capsaicin-pretreated rats, and thel-NAME effect was reversed by intravenous l- but notd-arginine. These findings indicate that vagal efferent activation induced by TRH analog injected intracisternally at a gastric acid secretory dose increases GMBF through atropine-sensitive mechanisms stimulatingl-arginine-nitric oxide pathways, whereas H1 receptors and capsaicin-sensitive afferent fibers do not play a role.

scholarly journals Dietary nitrate increases gastric mucosal blood flow and mucosal defense

2007 ◽  
Vol 292 (3) ◽  
pp. G718-G724 ◽  
Author(s):  
Joel Petersson ◽  
Mia Phillipson ◽  
Emmelie Å. Jansson ◽  
Andreas Patzak ◽  
Jon O. Lundberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Endothelial Nitric Oxide Synthase ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Dietary Nitrate ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Deficient Mice

Salivary nitrate from dietary or endogenous sources is reduced to nitrite by oral bacteria. In the acidic stomach, nitrite is further reduced to bioactive nitrogen oxides, including nitric oxide (NO). In this study, we investigated the gastroprotective role of nitrate intake and of luminally applied nitrite against provocation with diclofenac and taurocholate. Mucosal permeability (51Cr-EDTA clearance) and gastric mucosal blood flow (laser-Doppler flowmetry) were measured in anesthetized rats, either pretreated with nitrate in the drinking water or given acidified nitrite luminally. Diclofenac was given intravenously and taurocholate luminally to challenge the gastric mucosa. Luminal NO content and nitrite content in the gastric mucus were determined by chemiluminescence. The effect of luminal administration of acidified nitrite on the mucosal blood flow was also investigated in endothelial nitric oxide synthase-deficient mice. Rats pretreated with nitrate or given nitrite luminally had higher gastric mucosal blood flow than controls. Permeability increased more during the provocation in the controls than in the nitrate- and nitrite-treated animals. Dietary nitrate increased luminal NO levels 50 times compared with controls. Nitrate intake also resulted in nitrite accumulation in the loosely adherent mucous layer; after removal of this mucous layer, blood flow was reduced. Nitrite administrated luminally in endothelial nitric oxide synthase-deficient mice increased mucosal blood flow. We conclude that dietary nitrate and direct luminal application of acidified nitrite decrease diclofenac- and taurocholate-induced mucosal damage. The gastroprotective effect likely involves a higher mucosal blood flow caused by nonenzymatic NO production. These data suggest an important physiological role of nitrate in the diet.

Decreased endothelial nitric oxide synthase in gastric mucosa of rats with chronic renal failure

1998 ◽  
Vol 274 (6) ◽  
pp. F1102-F1108 ◽  
Author(s):  
M. Tomikawa ◽  
M. Ohta ◽  
N. D. Vaziri ◽  
J. D. Kaunitz ◽  
R. Itani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Chronic Renal Failure ◽  
Nitric Oxide Synthase ◽  
Gastric Mucosa ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Enos Mrna ◽  
Oxide Synthase

According to recent reports, chronic renal failure (CRF) increases the susceptibility of gastric mucosa to injury. Since nitric oxide plays a major role in gastric mucosal defense and injury, we investigated, in rats with CRF produced by five-sixths nephrectomy and in control rats, the expression of nitric oxide synthase (NOS) in the stomach and measured mucosal and submucosal gastric blood flow. In CRF rats, gastric mucosal blood flow was significantly reduced compared with control rats, whereas submucosal and serosal blood flow was significantly increased. CRF significantly decreased endothelial NOS (eNOS) mRNA abundance by 53% ( P < 0.01) and reduced expression of eNOS protein by 42% ( P < 0.01) compared with the controls. Enzyme activity of eNOS was significantly reduced in gastric mucosa of CRF rats ( P < 0.05). These data are consistent with reduced gastric mucosal blood flow in CRF rats and can explain altered susceptibility of gastric mucosa to injury in CRF rats.

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