The NO Donor Sodium Nitroprusside Reverses the Negative Effects on Hepatic Arterial Flow Induced by Endotoxin and the NO Synthase Inhibitor L-NAME

1996 ◽  
Vol 28 (5) ◽  
pp. 323-332 ◽  
Author(s):  
Y. Gundersen ◽  
T. Sætre ◽  
T. Scholz ◽  
H. Carlsen ◽  
H. Kjekshus ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
No Synthase ◽  
Arterial Flow ◽  
Negative Effects ◽  
Hepatic Arterial Flow ◽  
No Donor ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

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).

Influence of dipyridamole and its combination with NO donor or NO synthase inhibitor on adjuvant arthritis

2010 ◽  
Vol 10 (11) ◽  
pp. 1406-1414 ◽  
Author(s):  
Adel Gomaa ◽  
Mohsen Elshenawy ◽  
Noha Afifi ◽  
Eman Mohammed ◽  
Romany Thabit
Keyword(s):  
Adjuvant Arthritis ◽  
No Synthase ◽  
No Donor ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

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 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.

Relaxation induced by red wine polyphenolic compounds in rat pulmonary arteries: lack of inhibition by NO-synthase inhibitor

2008 ◽  
Vol 22 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Véronique Leblais ◽  
Stéphanie Krisa ◽  
Josep Valls ◽  
Arnaud Courtois ◽  
Sabrina Abdelouhab ◽  
...  
Keyword(s):  
Red Wine ◽  
Pulmonary Arteries ◽  
Polyphenolic Compounds ◽  
No Synthase ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

scholarly journals Erythropoietin Produces a Dual Effect on Carotid Body Chemoreception in Male Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Christian Arias-Reyes ◽  
Sofien Laouafa ◽  
Natalia Zubieta-DeUrioste ◽  
Vincent Joseph ◽  
Aida Bairam ◽  
...  
Keyword(s):  
Carotid Body ◽  
No Synthase ◽  
Male Rats ◽  
High Dose ◽  
No Production ◽  
Sprague Dawley ◽  
En Bloc ◽  
No Synthase Inhibitor ◽  
Sprague Dawley Rats ◽  
Synthase Inhibitor

Erythropoietin (EPO) regulates respiration under conditions of normoxia and hypoxia through interaction with the respiratory centers of the brainstem. Here we investigate the dose-dependent impact of EPO in the CB response to hypoxia and hypercapnia. We show, in isolated “en bloc” carotid body (CB) preparations containing the carotid sinus nerve (CSN) from adult male Sprague Dawley rats, that EPO acts as a stimulator of CSN activity in response to hypoxia at concentrations below 0.5 IU/ml. Under hypercapnic conditions, EPO did not influence the CSN response. EPO concentrations above 0.5 IU/ml decreased the response of the CSN to both hypoxia and hypercapnia, reaching complete inhibition at 2 IU/ml. The inhibitory action of high-dose EPO on the CSN activity might result from an increase in nitric oxide (NO) production. Accordingly, CB preparations were incubated with 2 IU/ml EPO and the unspecific NO synthase inhibitor (L-NAME), or the neuronal-specific NO synthase inhibitor (7NI). Both NO inhibitors fully restored the CSN activity in response to hypoxia and hypercapnia in presence of EPO. Our results show that EPO activates the CB response to hypoxia when its concentration does not exceed the threshold at which NO inhibitors masks EPO’s action.

Low protein diet exacerbates NO synthase inhibitor-induced hypertension in rats

1999 ◽  
Vol 3 (1) ◽  
pp. 34-40 ◽  
Author(s):  
H. Kumagai ◽  
Yoshiko Kikuchi ◽  
Noriko Kumeta ◽  
Masato Kimura ◽  
Toshio Sakai
Keyword(s):  
No Synthase ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein ◽  
No Synthase Inhibitor ◽  
Induced Hypertension ◽  
Synthase Inhibitor
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