Detection and Description of Various Stores of Nitric Oxide Store in Vascular Wall

Vlasova, M. A.; Vanin, Anatoly F.; Müller, Bernard; Smirin, Boris V.; Malyshev, I. Yu.; Манухина, Е. Б.

doi:10.1023/b:bebm.0000008969.39841.34

Cited by 14 publications

(14 citation statements)

References 8 publications

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“…NO and NO‐derived oxidant are important messengers that play role in physiological and pathological processes such as apoptosis, vasorelaxation and inflammation [37,38]. It is now established that ceramide generation is regulated either positively or negatively by NO and NO reactive species [39].…”

Section: Resultsmentioning

confidence: 99%

The relation between sphingomyelinase activity, lipid peroxide oxidation and NO‐releasing in mice liver and brain

et al. 2005

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We used animal models to study connection between oxidating system and sphingomyelin signaling cascade, because this models are more close related to people disease. Activation of n-sphingomyelinase (n-SMase) in mice liver and brain is coincided in time with increased level of peroxide products (conjugated dienes) after injection of tumor necrosis factor a (TNF-a). We found that ceramide can induce peroxide oxidation and lead to accumulation of TNF-a in animal organs. Nitric oxide (NO) donors (S-nitrosoglutathione and dinitrosyl iron complex) reversibly inhibited activity of n-SMase and decreased level of lipid peroxidation products. This data proposed that both SMase and messengers of oxidative systems could be targets for NO-derived oxidants.

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Section: Resultsmentioning

confidence: 99%

The relation between sphingomyelinase activity, lipid peroxide oxidation and NO‐releasing in mice liver and brain

et al. 2005

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“…143 NO can be bound into S-nitrosothiols and dinitrosyl iron complexes for transport and intracellular storage. [147][148][149] These NO stores are formed with any increase in NO, so by sequestering excess free NO, these stores can provide protection by buffering NO overproduction. On the other hand, when NO production is deficient, NO stores can be mobilized to provide an additional NO source.…”

Section: Intermittent Hypoxic Training (Iht) Improves Cerebrovascularmentioning

confidence: 99%

Intermittent hypoxia training protects cerebrovascular function in Alzheimer's disease

Манухина

Downey

Shi

et al. 2016

Exp Biol Med (Maywood)

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Alzheimer's disease (AD) is a leading cause of death and disability among older adults. Modifiable vascular risk factors for AD (VRF) include obesity, hypertension, type 2 diabetes mellitus, sleep apnea, and metabolic syndrome. Here, interactions between cerebrovascular function and development of AD are reviewed, as are interventions to improve cerebral blood flow and reduce VRF. Atherosclerosis and small vessel cerebral disease impair metabolic regulation of cerebral blood flow and, along with microvascular rarefaction and altered trans-capillary exchange, create conditions favoring AD development. Although currently there are no definitive therapies for treatment or prevention of AD, reduction of VRFs lowers the risk for cognitive decline. There is increasing evidence that brief repeated exposures to moderate hypoxia, i.e. intermittent hypoxic training (IHT), improve cerebral vascular function and reduce VRFs including systemic hypertension, cardiac arrhythmias, and mental stress. In experimental AD, IHT nearly prevented endothelial dysfunction of both cerebral and extra-cerebral blood vessels, rarefaction of the brain vascular network, and the loss of neurons in the brain cortex. Associated with these vasoprotective effects, IHT improved memory and lessened AD pathology. IHT increases endothelial production of nitric oxide (NO), thereby increasing regional cerebral blood flow and augmenting the vaso-and neuroprotective effects of endothelial NO. On the other hand, in AD excessive production of NO in microglia, astrocytes, and cortical neurons generates neurotoxic peroxynitrite. IHT enhances storage of excessive NO in the form of S-nitrosothiols and dinitrosyl iron complexes. Oxidative stress plays a pivotal role in the pathogenesis of AD, and IHT reduces oxidative stress in a number of experimental pathologies. Beneficial effects of IHT in experimental neuropathologies other than AD, including dyscirculatory encephalopathy, ischemic stroke injury, audiogenic epilepsy, spinal cord injury, and alcohol withdrawal stress have also been reported. Further research on the potential benefits of IHT in AD and other brain pathologies is warranted.

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“…Moreover, the nonheme Fe(III)-or Fe(II)-NO complex may be present in the low molecular weight iron pool near the endothelial luminal membrane for the donation of NO (Cooper, 1999;Alencar et al, 2003;Vlasova et al, 2003).…”

Section: ) Capillary Endothelial Cellsmentioning

confidence: 99%

Cellular and subcellular localizations of nonheme ferric and ferrous iron in the rat brain: a light and electron microscopic study by the perfusion-Perls and -Turnbull methods

Meguro

Asano

Odagiri

et al. 2008

Archives of Histology and Cytology

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Detection and Description of Various Stores of Nitric Oxide Store in Vascular Wall

Cited by 14 publications

References 8 publications

The relation between sphingomyelinase activity, lipid peroxide oxidation and NO‐releasing in mice liver and brain

The relation between sphingomyelinase activity, lipid peroxide oxidation and NO‐releasing in mice liver and brain

Intermittent hypoxia training protects cerebrovascular function in Alzheimer's disease

Cellular and subcellular localizations of nonheme ferric and ferrous iron in the rat brain: a light and electron microscopic study by the perfusion-Perls and -Turnbull methods

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