Therapeutic role of nitric oxide as emerging molecule

Kumar, Sahil; Singh, Rajesh; Bhardwaj, T. R.

doi:10.1016/j.biopha.2016.11.125

Cited by 81 publications

(61 citation statements)

References 159 publications

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“…Nitrates have also been found to have anti-inflammatory effects via NO’s role in the inflammatory process (91). Nitric oxide inhibits neutrophil adhesion and chemotaxis in acute inflammation and modulates microvascular permeability (92–95).…”

Section: Non-hemodynamic Effects Of Nitratesmentioning

confidence: 99%

The Role of Nitroglycerin and Other Nitrogen Oxides in Cardiovascular Therapeutics

Divakaran

Loscalzo

2017

Journal of the American College of Cardiology

119

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The use of nitroglycerin in the treatment of angina pectoris began not long after its original synthesis in 1847. Since then, the discovery of nitric oxide as a biological effector and better understanding of its roles in vasodilation, cell permeability, platelet function, inflammation, and other vascular processes have advanced our knowledge of the hemodynamic (mostly mediated through vasodilation of capacitance and conductance arteries) and non-hemodynamic effects of organic nitrate therapy, via both nitric oxide-dependent and independent mechanisms. Nitrates are rapidly absorbed from mucous membranes, the gastrointestinal tract, and the skin, and, thus, nitroglycerin is available in several preparations for delivery via several routes: oral tablets, sublingual tablets, buccal tablets, sublingual spray, transdermal ointment, and transdermal patch; it is also available in intravenous formulations. The organic nitrates are commonly used in the treatment of cardiovascular disease, but clinical data limit their use mostly to the treatment of angina. They are also used in the treatment of subsets of patients with heart failure and pulmonary hypertension. One major problem with the use of nitrates is the development of tolerance. Although several agents have been studied for use in the prevention of nitrate tolerance, none are currently recommended owing to a paucity of supportive clinical data. Only one method of preventing nitrate tolerance remains widely accepted: the use of a dosing strategy that provides an interval of no or low nitrate exposure during each 24-hour period. Nitric oxide’s important role in several cardiovascular disease mechanisms continues to drive research toward finding novel ways to affect both endogenous and exogenous sources of this key molecular mediator.

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Section: Non-hemodynamic Effects Of Nitratesmentioning

confidence: 99%

The Role of Nitroglycerin and Other Nitrogen Oxides in Cardiovascular Therapeutics

Divakaran

Loscalzo

2017

Journal of the American College of Cardiology

119

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“…Це вільнорадикальна молекула, що продукується in vivo у регульованому ферментативному процесі з Lаргініну за допомогою родини NO-синтаз (NOS). NO модулює широкий спектр сигнальних шляхів практично в усіх органах і системах організму, включаючи вазоділатацію, нейрональну трансмісію, імуномодуляцію, сердцеве скорочення, інгібування агрега-ції тромбоцитів, диференціювання та проліферацію стовбурових клітин (Lei, 2013;Cossenza & Socodato, 2014;Kumar, 2017). У гастродуоденальній зоні NO стимулює секрецію слизу за допомогою активації гуанілатциклази в епітеліальних клітинах (Lundberg & Weitzberg, 2012;Tkach et al, 2013).…”

Section: вступunclassified

Cytoprotective processes induced by the effect of L-arginin-L-glutamate in rats with experimental pathology of the gastroduodenal zone

Stepanov

Ponomarenko

Lykholat

et al. 2018

Regul. Mech. Biosyst.

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2018). Cytoprotective processes induced by the effect of L-arginin-L-glutamate in rats with experimental pathology of the gastroduodenal zone.The processes of effect of L-arginine-L-glutamate on peroxidation and slime-forming function of the stomach cells, the system of antioxidant defense in the blood, liver and brain tissues of rats with experimental pathology of the gastroduodenal zone have been investigated. The animals were divided into four groups. Group I -control group were rats injected intragastrically through a probe physiological solution. Group II included animals with erosive ulcerative lesions of the gastroduodenal zone. Modeling of the erosive ulcerative lesions was carried out by intragastric administration of medical bile (1 ml/100 g) in combination with immobilization-cold stress for 1 hour at + 4 ºС for a period of seven days. Rats of group ІІІ simultaneously received an intra-abdominal 4% solution of L-arginine-L-glutamate in a dose of 20 mg per 100 g of body weight at the same time as the erosive ulcerative lesions modeling. To clarify the role of NO-ergic mechanism of L-arginine-Lglutamate influence on the quantitative composition of mucins and free radical processes rats in group ІV with erosive ulcerative lesions were injected with non-selective NO-synthase inhibitor, L-NAME (L-NG-nitroarginine methyl ester), at a dose of 1 mg per 100 g at the same time as injections of 4% solution of L-arginine-L-glutamate. The simulation of erosiveulcerative lesions of the gastroduodenal zone in the experimental animals was accompanied by the intensification of lipid peroxidation processes, the imbalance of the antioxidant defense systems and the development of oxidative stress in the blood, tissues of the stomach, liver and brain, which has tissue-specific features. In the blood of the animals, the activation of the enzymatic link of antioxidant defense did not compensate for free radical processes, as a result, the exhaustion of the reduced glutathione pool occurred, and the level of TBA-active products increased both in plasma and in erythrocytes. There was a depression of the enzymes of the antioxidant defense and a decrease in the level of recovered glutathione, indicating decompensating of the liver antioxidant protection systems in the liver tissue of the rats. In the experimental animals , formation of erosive ulcerative lesions was accompanied by destabilization of the oxidation-reducing processes in the brain, which led to the intensification of the lipoperoxidation. In the mucous membrane of the stomach of the experimental animals, the total number of protection factors -secretory mucins with a simultaneous structural change -decreased. The use of L-arginine-Lglutamate reduced the manifestations of oxidative stress in the stomach tissue of animals with experimental pathology and normalized the quantitative and qualitative composition of mucins. In the blood, liver tissues and brain of the rats, L-arginine-Lglutamate injections activated the enzymes of the first anti-radical linkage -superoxid...

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Section: Introductionmentioning

confidence: 99%

“…Endogenous NO is synthesized from the precursor, l ‐arginine, by 3 NO synthase (NOS) enzymes, viz endothelial NOS, neuronal NOS and inducible NOS . Under normal conditions in vivo, NO is a highly diffusible gas with a half‐life of only a few seconds that regulates many physiological processes . However, after peripheral nerve injury, ongoing ectopic firing of injured primary afferents induces central sensitization in the dorsal horn of the spinal cord that is underpinned by persistent activation of the N ‐methyl‐ d ‐aspartate (NMDA)/NOS/NO signaling cascade and glial cell activation, to markedly increase NO formation at multiple levels of the somatosensory nervous system .…”

Section: Introductionmentioning

confidence: 99%

“…7 Under normal conditions in vivo, NO is a highly diffusible gas with a half-life of only a few seconds that regulates many physiological processes. 7 However, after peripheral nerve injury, ongoing ectopic firing of injured primary afferents induces central sensitization in the dorsal horn of the spinal cord that is underpinned by persistent activation of the N-methyld-aspartate (NMDA)/NOS/NO signaling cascade and glial cell activation, to markedly increase NO formation at multiple levels of the somatosensory nervous system. [8][9][10] In diabetes, there is increased generation of superoxide that reacts with elevated levels of NO to increase formation of the neurotoxin, peroxynitrite, resulting in nitrooxidative stress and the development of PDN.…”

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confidence: 99%

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Morphine hyposensitivity in streptozotocin‐diabetic rats: Reversal by dietary l‐arginine treatment

Lotfipour

Smith

2017

Clin Exp Pharma Physio

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SummaryPainful diabetic neuropathy (PDN) is a long-term complication of diabetes. Defining symptoms include mechanical allodynia (pain due to light pressure or touch) and morphine hyposensitivity. In our previous work using the streptozotocin (STZ)-diabetic rat model of PDN, morphine hyposensitivity developed in a temporal manner with efficacy abolished at 3 months post-STZ and maintained for 6 months post-STZ. As this time course mimicked that for the temporal development of hyposensitivity to the pain-relieving effects of the furoxan nitric oxide (NO) donor, PRG150 (3-methylfurox an-4-carbaldehyde) in STZ-diabetic rats, we hypothesized that progressive depletion of endogenous NO bioactivity may underpin the temporal loss of morphine sensitivity in STZ-diabetic rats. Furthermore, we hypothesized that replenishment of NO bioactivity may restore morphine sensitivity in these animals. Diabetes was induced in male Dark Agouti rats by intravenous injection of STZ (85 mg/kg). Diabetes was confirmed on day 7 if blood glucose concentrations were ≥15 mmol/L. Mechanical allodynia was fully developed in the bilateral hindpaws by 3 weeks of STZ-diabetes in rats and this was maintained for the study duration. Morphine hyposensitivity developed in a temporal manner with efficacy abolished by 3 months post-STZ. Administration of dietary l-arginine (NO precursor) at 1 g/d to STZ-diabetic rats according to a 15-week prevention protocol initiated at 9 weeks post-STZ prevented abolition of morphine efficacy. When given as an 8-week intervention protocol in rats where morphine efficacy was abolished, dietary l-arginine at 1 g/d progressively rescued morphine efficacy and potency. Our findings implicate NO depletion in the development of morphine hyposensitivity in STZ-diabetic rats. K E Y W O R D Sintervention protocol, l-arginine, mechanical allodynia morphine, morphine hyposensitivity, nitric oxide, painful diabetic neuropathy, prevention protocol, STZ-diabetic rats | INTRODUCTIONPainful diabetic neuropathy (PDN) is a type of peripheral neuropathic pain that develops in the long nerves in a "stocking and glove" distribution, and that affects up to 20% of patients with diabetes.1,2 PDN symptoms include lancinating, burning and shooting pains as well as mechanical allodynia, a type of pain evoked by non-noxious mechanical stimuli such as light pressure or touch. 1,2 In our previous work, we showed that single bolus doses of the furoxan nitric oxide (NO) donor, PRG150 (3-methylfuroxan-4-carbaldehyde), evoked dose-dependent pain relief in STZ-diabetic rats. However, the efficacious bolus doses of PRG150 at 14 and 24 weeks of STZ-diabetes were 3 to 4 orders of magnitude higher than that required at 10 weeks post-STZ or in nondiabetic control rats. In other work by our group in diabetic rats assessed in longitudinal studies over prolonged periods, morphine hyposensitivity

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Therapeutic role of nitric oxide as emerging molecule

Cited by 81 publications

References 159 publications

The Role of Nitroglycerin and Other Nitrogen Oxides in Cardiovascular Therapeutics

The Role of Nitroglycerin and Other Nitrogen Oxides in Cardiovascular Therapeutics

Cytoprotective processes induced by the effect of L-arginin-L-glutamate in rats with experimental pathology of the gastroduodenal zone

Morphine hyposensitivity in streptozotocin‐diabetic rats: Reversal by dietary l‐arginine treatment

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