The role of nitric oxide in cardiovascular diseases

Naseem, Khalid M.

doi:10.1016/j.mam.2004.09.003

Cited by 456 publications

(349 citation statements)

References 170 publications

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“…The vascular endothelial cells transduce circulatory stimuli to the arterial wall leading to the regulation of vascular tone, haemostasis, blood pressure and vascular remodeling through the synthesis and release of vasoactive NO [51,52]. NO is synthesized by the conversion of Larginine to L-citrulline by the enzyme of nitric oxide synthase (NOS) which exists in three isoforms in brain: eNOS localized in endothelial cells; nNOS localized in neurons; and inducible NOS (iNOS) induced in neurons and glial cells after cytokine activation [51,52] [58].…”

Section: Nitric Oxide Malfunction and Vascular Oxidative Stress In Almentioning

confidence: 99%

“…Once formed, peroxynitrite can nitrate tyrosine residues to form nitrotyrosine. Additionally, substantial amounts of ONOO-can be protonated at physiological pH to form peroxynitrous acid, a strong oxidant itself, which in turn can yield the highly reactive OH•, a much more powerful oxidant that will readily react with any biological molecules it meets [51,52].Increased nitrotyrosine is found in astrocytes, blood vessels and the neuronal cytoplasm of the cerebral cortex within regions of neurodegeneration in AD, yet it is undetectable in corresponding control regions [24,59,60]. There is also a significant two-to three-fold increase in the lipid nitration product, 5-nitro-γ-tocopherol, in affected regions of the brain in AD, suggesting NO is a significant contributor to lipid oxidation [61].…”

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confidence: 99%

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Vascular oxidative stress in Alzheimer disease

Zhu

Smith

Honda

et al. 2007

Journal of the Neurological Sciences

159

156

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Alzheimer disease and cerebrovascular dementia are two common causes of dementia and, by present diagnostic criteria, are mutually exclusive using vascular pathology as an arbitrary demarcation in differential diagnosis. However, evidence from epidemiological, neuropathological, clinical, pharmacological, and functional studies suggest considerable overlap in risk factors and pathological changes suggesting shared common pathogenic mechanisms between these two diseases such that vascular factors play a vital role in the pathogenesis of Alzheimer disease. A high energy demand and lack of an endogenous fuel reserve make the brain highly dependent upon a continuous blood supply where disruption of cerebral blood vessels and blood flow can have serious consequences on neural activities. Indeed, many studies implicate metabolic defects in Alzheimer disease, such a reduced brain metabolism is one of the best documented abnormalities in the disease. Notably, since endothelial reactive oxygen species such as nitric oxide act as vasodilators at low concentrations, increased production coupled with elevated reactive oxygen species scavenging of nitric oxide, can lead to reduced bioavailability of nitric oxide and increased oxidative stress that damage sensitive vascular cells. In this respect, we and others have demonstrated that oxidative stress is one of the earliest pathological changes in the brain of Alzheimer disease patients and plays a critical role in the vascular abnormalities underlying metabolic defects in Alzheimer disease. Here, we discuss vascular factors in relation to Alzheimer disease and review hypoperfusion as a potential cause by triggering mitochondrial dysfunction and increased oxidative stress initiating the pathogenic process. KeywordsAlzheimer disease; hypoperfusion; mitochondria; nitric oxide; nitric oxide synthase; oxidative stress; vascular abnormalitiesCorrespondence to: George Perry, Ph.D., College of Sciences, University of Texas at San Antonio, 6900 North Loop 1604 West, San Antonio, Texas 78249-0661 USA, , george.perry@utsa.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. . Therefore, perivascular Aβ deposits may be a risk factor for reduced regional CBF [7]. Ultrastructural studies on blood vessels associated with Aβ deposits have shown their intermittent association with membrane abnormalities of smooth muscle cells [5]. Indeed, in AD cases with a clinical history of cerebral bleeding, the muscle layer is sometimes completely replaced by Aβ deposits, suggesting that the vascular system may be an initiator for the development of diseas...

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Section: Nitric Oxide Malfunction and Vascular Oxidative Stress In Almentioning

confidence: 99%

mentioning

confidence: 99%

Vascular oxidative stress in Alzheimer disease

Zhu

Smith

Honda

et al. 2007

Journal of the Neurological Sciences

159

156

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“…In this study we focused on NO and NFkB as target molecules because there is substantial evidence that they play key roles in atherogenesis (see Naseem, 2005;de Winther et al, 2005). We examined whether these molecules are influenced by the soy isoflavones genistein and daidzein.…”

Section: No Concentrationmentioning

confidence: 99%

Techniques for quantifying effects of dietary antioxidants on transcription factor translocation and nitric oxide production in cultured cells

et al. 2006

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“…Reduced bioavailability of NO is thought to be one of the central factors common to cardiovascular disease, although it is unclear whether this is a cause of, or result of, endothelial dysfunction. Any disturbance in the bioavailability of NO leads to a loss of cardio protective actions and in some cases may even increase disease progression [1].…”

Section: Introductionmentioning

confidence: 99%

Biochemistry of Nitric Oxide

2011

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Nitric oxide (NO) a free radical having both cytoprotective as well as tumor promoting agent is formed from L-arginine by converting it to L-citrulline via nitric oxide synthase enzymes. The reaction product of nitric oxide with superoxide generates potent oxidizing agent, peroxynitrite which is the main mediator of tissue and cellular injury. Peroxynitrite is reactive towards many biomolecules which includes amino acids, nucleic acid bases; metal containing compounds, etc. NO metabolites may play a key role in mediating many of the genotoxic/ carcinogenic effects as DNA damage, protein or lipid modification, etc. The basic reactions of nitric oxide can be divided as direct effect of the radical where it alone plays a role in either damaging or protecting the cell milieu and an indirect effect in which the byproducts of nitric oxide formed by convergence of two independent radical generating pathways play the role in biological reactions which mainly involve oxidative and nitrosative stress. Nitric oxide is also capable of directly interacting with mitochondria through inhibition of respiration or by permeability transition. Reaction of nitric oxide with metal ions include its direct interaction with the metals or with oxo complexes thereby reducing them to lower valent state. Excessive production of nitric oxide can be studied by inhibiting the synthetic pathway of nitric oxide using both selective or specific nitric oxide synthase inhibitor or nonselective nitric oxide synthase inhibitor with respect to isoforms of nitric oxide.Keywords Nitric oxide Á Nitric oxide synthase Á Nitric oxide inhibitors Á Generation of nitric oxide Á Cancer Á Systemic lupus erythematosus Á Direct and indirect effect of nitric oxide Á Effect of nitric oxide on mitochondria

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The role of nitric oxide in cardiovascular diseases

Cited by 456 publications

References 170 publications

Vascular oxidative stress in Alzheimer disease

Vascular oxidative stress in Alzheimer disease

Techniques for quantifying effects of dietary antioxidants on transcription factor translocation and nitric oxide production in cultured cells

Biochemistry of Nitric Oxide

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