scholarly journals Protective effect of dietary nitrate on experimental gastritis in rats

2003 ◽  
Vol 89 (6) ◽  
pp. 777-786 ◽  
Author(s):  
Muriel Larauche ◽  
Pauline M. Anton ◽  
Rafaël Garcia-Villar ◽  
Vassilia Theodorou ◽  
Jacques Frexinos ◽  
...  
Keyword(s):  
Protective Effect ◽  
Sodium Nitroprusside ◽  
Human Health ◽  
Mucosal Damage ◽  
Normal Diet ◽  
No Synthase ◽  
Gastric Mucosal Damage ◽  
No Donor ◽  
Dietary Nitrate ◽  
Synthase Inhibitor

Nitrates have long been considered as harmful dietary components and judged responsible for deleterious effects on human health, leading to stringent regulations concerning their levels in food and water. However, recent studies demonstrate that dietary nitrate may have a major role in human health as a non-immune mechanism for host defence, through its metabolism to NO in the stomach. NO is a versatile molecule and although evidence exists showing that administration of low doses of exogenous NO protects against gastrointestinal inflammation, higher NO doses have been shown to exacerbate injury. So, the effect of an ingestion of nitrates in doses corresponding to a normal diet in human consumers on an experimental gastritis induced by iodoacetamide in rats was investigated. During gastritis one of the following compounds was given orally: water; KNO3; the NO donor sodium nitroprusside; the NO scavenger haemoglobin given with either water or KNO3. N(G)-nitro-L-arginine methyl ester (L-NAME), a non-specific NO synthase inhibitor, was administered with either water, iodoacetamide alone, or combined with KNO3. After killing, the stomach was resected and microscopic damage scores, myeloperoxidase and NO synthase activities were determined. Iodoacetamide-induced gastritis was significantly reduced by KNO3administration, an effect which was reproduced by sodium nitroprusside and reversed by haemoglobin. L-NAME induced gastric mucosal damage in itself, and KNO3did not prevent the gastritis induced by iodoacetamide associated with L-NAME. In conclusion, dietary nitrate exerts a protective effect against an experimental gastritis in rats by releasing NO in the stomach but such an effect requires the production of endogenous NO.

scholarly journals Nitric Oxide Ameliorates Plant Metal Toxicity by Increasing Antioxidant Capacity and Reducing Pb and Cd Translocation

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1981
Author(s):  
Abolghassem Emamverdian ◽  
Yulong Ding ◽  
James Barker ◽  
Farzad Mokhberdoran ◽  
Muthusamy Ramakrishnan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heavy Metal ◽  
Sodium Nitroprusside ◽  
Metal Toxicity ◽  
Heavy Metal Toxicity ◽  
No Synthase ◽  
Bamboo Species ◽  
No Donor ◽  
Cd Toxicity ◽  
Synthase Inhibitor

Recently, nitric oxide (NO) has been reported to increase plant resistance to heavy metal stress. In this regard, an in vitro tissue culture experiment was conducted to evaluate the role of the NO donor sodium nitroprusside (SNP) in the alleviation of heavy metal toxicity in a bamboo species (Arundinaria pygmaea) under lead (Pb) and cadmium (Cd) toxicity. The treatment included 200 µmol of heavy metals (Pb and Cd) alone and in combination with 200 µM SNP: NO donor, 0.1% Hb, bovine hemoglobin (NO scavenger), and 50 µM L-NAME, N(G)-nitro-L-arginine methyl ester (NO synthase inhibitor) in four replications in comparison to controls. The results demonstrated that the addition of L-NAME and Hb as an NO synthase inhibitor and NO scavenger significantly increased oxidative stress and injured the cell membrane of the bamboo species. The addition of sodium nitroprusside (SNP) for NO synthesis increased antioxidant activity, protein content, photosynthetic properties, plant biomass, and plant growth under heavy metal (Pb and Cd) toxicity. It was concluded that NO can increase plant tolerance for metal toxicity with some key mechanisms, such as increasing antioxidant activities, limiting metal translocation from roots to shoots, and diminishing metal accumulation in the roots, shoots, and stems of bamboo species under heavy metal toxicity (Pb and Cd).

scholarly journals Permissive contributions of NO and prostacyclin in CO-induced cerebrovascular dilation in piglets

2005 ◽  
Vol 289 (1) ◽  
pp. H432-H438 ◽  
Author(s):  
Charles W. Leffler ◽  
Alexander L. Fedinec ◽  
Helena Parfenova ◽  
Jonathan H. Jaggar
Keyword(s):  
Sodium Nitroprusside ◽  
Phosphodiesterase Inhibitor ◽  
Cerebrovascular Circulation ◽  
No Synthase ◽  
Common Mechanism ◽  
No Donor ◽  
Cerebral Arterioles ◽  
Newborn Pigs ◽  
Synthase Inhibitor ◽  
Prostacyclin Analog

Endogenously produced CO is an important dilator in newborn cerebrovascular circulation. CO dilates cerebral arterioles by activating Ca2+-activated K+ channels, but modulatory actions of other effectors and second messenger inputs are unclear. Specifically, the mechanisms behind the obligatory permissive roles of prostacyclin and NO are uncertain. Therefore, the present study was performed using acutely implanted, closed cranial windows in newborn pigs to address the hypothesis that the permissive roles of NO and prostacyclin in cerebrovascular dilation in response to CO involve a common mechanism. The NO donor sodium nitroprusside restored dilation in response to CO after inhibition of that dilation with the prostaglandin cyclooxygenase inhibitor indomethacin. The stable prostacyclin analog iloprost restored CO-induced dilation blocked by the NO synthase inhibitor Nω-nitro-l-arginine. Restoration of dilation in response to CO by the cGMP-dependent phosphodiesterase inhibitor zaprinast and blockade of CO dilation by the guanylyl cyclase inhibitor 1 H-[1,2,4]oxadiazole-[4,3- a]quinoxalin-1-one (ODQ) suggests involvement of the cGMP/PKG pathway. Iloprost or the cAMP-dependent dilator isoproterenol restored dilation in response to CO after ODQ administration. However, CO-induced dilation blocked by the cGMP-dependent PKG inhibitor Rp-8-[(4-chlorophenyl)thio]-cGMPS triethylamine could not be reversed by administration of sodium nitroprusside, iloprost, or isoproterenol. Conversely, PKA inhibition did not block dilation in response to CO. Overall, data indicate that activation of PKG is the predominant mechanism of the permissive actions of NO and prostacyclin for CO-induced pial arteriolar dilation.

scholarly journals Protective Effect of Sodium Nitroprusside on the Rat Small Intestine Transplanted Mucosa

2015 ◽  
Vol 2015 ◽  
pp. 1-6
Author(s):  
Feng-Hua Chen ◽  
Ke Li ◽  
Lu Yin ◽  
Chun-Qiu Chen ◽  
Zhao-Wen Yan ◽  
...  
Keyword(s):  
Small Intestine ◽  
Molecular Markers ◽  
Protective Effect ◽  
Sodium Nitroprusside ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Small Bowel Transplantation ◽  
Mucosal Barrier ◽  
No Donor

The intestinal mucosal epithelium is extremely susceptible to even brief periods of ischemia. Mucosal barrier damage, which is associated with ischemia/reperfusion (I/R) injury and consequently bacterial translocation, remains a major obstacle for clinically successful small bowel transplantation (SBT). Previous studies have demonstrated a protective effect of nitric oxide (NO) on other transplanted organs and NO mediated intestinal protection has also been reportedin vitro. The aim of this study was to evaluate the effect of sodium nitroprusside (SNP), NO donor, on graft mucosal histology and molecular markers of function after SBT in rats. We used SNP in different period of heterotopic SBT rats. The groups consisted of SBT, pre-SNP group, and post-SNP group. Interestingly, the pre-SNP graft samples exhibited less damage compared to the SBT and post-SNP samples. In addition, mucosal samples from the pre-SNP group showed higher Na+-K+-ATPase activity and higher levels of laminin expression compared to the SBT and post-SNP samples. The findings of the present study reveal that SNP given before graft ischemia/reperfusion injury has a protective effect on mucosal histology and molecular markers of function in the transplanted small intestine.

Potassium channel-mediated vasorelaxation is impaired in experimental renal failure

1999 ◽  
Vol 277 (4) ◽  
pp. H1622-H1629 ◽  
Author(s):  
Jarkko Kalliovalkama ◽  
Pasi Jolma ◽  
Jari-Petteri Tolvanen ◽  
Mika Kähönen ◽  
Nina Hutri-Kähönen ◽  
...  
Keyword(s):  
Renal Failure ◽  
No Synthase ◽  
Sham Operation ◽  
No Donor ◽  
Plasma Urea ◽  
Failure Group ◽  
The Difference ◽  
Wistar Kyoto ◽  
Synthase Inhibitor ◽  
Experimental Renal Failure

Chronic renal failure is associated with increased cardiovascular morbidity and abnormal arterial tone, but the underlying pathophysiological mechanisms are poorly understood. Therefore, we studied the responses of isolated mesenteric arterial rings from Wistar-Kyoto rats in standard organ chambers 6 wk after subtotal (5/6) nephrectomy or sham operation. Subtotal nephrectomy resulted in a 1.7-fold elevation of plasma urea nitrogen, whereas blood pressure was not significantly affected. Endothelium-mediated relaxations of norepinephrine-precontracted rings to ACh were impaired in renal failure rats. The nitric oxide (NO) synthase inhibitor N G-nitro-l-arginine methyl ester inhibited relaxations to ACh more effectively in the renal failure group, whereas the cyclooxygenase inhibitor diclofenac did not significantly affect the response in either group. Inhibition of Ca2+-activated K+ channels by charybdotoxin and apamin attenuated NO synthase- and cyclooxygenase-resistant relaxations to ACh in control but not renal failure rats and abolished the difference between these groups. Endothelium-independent relaxations to isoproterenol and cromakalim, vasodilators acting via β-adrenoceptors and ATP-sensitive K+ channels, respectively, were impaired in the renal failure group, whereas relaxations to the NO donor nitroprusside were similar in both groups. In conclusion, endothelium-mediated relaxation in renal failure rats was impaired in the absence and presence of NO synthase and cyclooxygenase inhibition but not with prevented smooth muscle hyperpolarization. Endothelium-independent relaxations to isoproterenol and cromakalim were also attenuated after 5/6 nephrectomy. These results suggest that impaired vasodilatation in experimental renal failure could be attributed to reduced relaxation via arterial K+ channels.

Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?

1995 ◽  
Vol 268 (2) ◽  
pp. G207-G214 ◽  
Author(s):  
A. Rodriguez-Membrilla ◽  
V. Martinez ◽  
M. Jimenez ◽  
E. Gonalons ◽  
P. Vergara
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Motor Pattern ◽  
No Synthase ◽  
Phase Iii ◽  
Motor Patterns ◽  
No Donor ◽  
Postprandial State ◽  
Synthase Inhibitor

The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.

scholarly journals Protective effect of dicloguamine maleate (MN-1695) on HCl-induced gastric mucosal damage in rats-Histologic studies.

1987 ◽  
Vol 89 (5) ◽  
pp. 279-284 ◽  
Author(s):  
Fusao UEDA ◽  
Takashi KYOI ◽  
Kiyoshi KIMURA ◽  
Hiroshi ENOMOTO
Keyword(s):  
Protective Effect ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage
Sign in / Sign up

Export Citation Format

Share Document