Cardiovascular Effects of Peroxynitrite

Uppu, Rao M.; Nossaman, Bobby D.; Greco, Anthony J.; Fokin, Alex; Murthy, Subramanyam N.; Fonseca, Vivian; Kadowitz, Philip J.

doi:10.1111/j.1440-1681.2007.04641.x

Cited by 41 publications

(30 citation statements)

References 53 publications

(147 reference statements)

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“…ONOO Ϫ has been shown to trigger apoptosis in cardiomyocytes as well as in endothelial and vascular smooth muscle cells, induces the up-regulation of adhesion molecules in endothelial cells, the disruption of endothelial glycocalyx, and may enhance the adhesion of neutrophils to the endothelium. 35 This effect of MS MPs on endothelial cells may explain the dissociation between reduced NO and O 2 Ϫ formation in cultured endothelial cells, and may account for endothelial dysfunction.…”

Section: /Cd42bmentioning

confidence: 99%

Endothelial Dysfunction Caused by Circulating Microparticles from Patients with Metabolic Syndrome

Agouni

Lagrue-Lak-Hal

Ducluzeau

et al. 2008

The American Journal of Pathology

252

209

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Microparticles are membrane vesicles that are released during cell activation and apoptosis. Elevated levels of microparticles occur in many cardiovascular diseases; therefore, we characterized circulating microparticles from both metabolic syndrome (MS) patients and healthy patients. We evaluated microparticle effects on endothelial function; however, links between circulating microparticles and endothelial dysfunction have not yet been demonstrated. Circulating microparticles and their cellular origins were examined by flow cytometry of blood samples from patients and healthy subjects. Microparticles were used either to treat human endothelial cells in vitro or to assess endothelium function in mice after intravenous injection. MS patients had increased circulating levels of microparticles compared with healthy patients, including microparticles from platelet, endothelial, erythrocyte, and procoagulant origins. In vitro treatment of endothelial cells with microparticles from MS patients reduced both nitric oxide (NO) and superoxide anion production, resulting in protein tyrosine nitration. These effects were associated with enhanced phosphorylation of endothelial NO synthase at the site of inhibition. The reduction of O 2 ؊ was linked to both reduced expression of p47 phox of NADPH oxidase and overexpression of extracellular superoxide dismutase. The decrease in NO production was triggered by nonplatelet-derived microparticles. In vivo injection of MS microparticles into mice impaired endothelium-dependent relaxation and decreased endothelial NO synthase expression. These data provide evidence that circulating microparticles from MS patients influence endothelial dysfunction. (Am J Pathol

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Section: /Cd42bmentioning

confidence: 99%

Endothelial Dysfunction Caused by Circulating Microparticles from Patients with Metabolic Syndrome

Agouni

Lagrue-Lak-Hal

Ducluzeau

et al. 2008

The American Journal of Pathology

252

209

View full text Add to dashboard Cite

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“…GSH plays important role in maintenance of NO pool. GSH reacts with peroxynitrite to produce Snitrosoglutathione (GSNO) which extends the half-life of NO and in consequence contributes in relaxation of vascular tissue [20]. GSH enhances decomposition of nitrosothiols and release of NO [21].…”

Section: Discussionmentioning

confidence: 99%

Glutathione concentration, glutathione peroxidase and glutathione reductase activity in elderly patients with type II diabetes compared to hypertensives

Rybka

Kupczyk

Kędziora–Kornatowska

et al. 2010

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“…In addition, exhaled NO can be measured as a marker of asthma and other inammatory lung diseases. In this review, we discuss the role of NO in hypertension as well 5 as the targets of NO .…”

Section: General Backgroundmentioning

confidence: 99%

“…the [Ca ]i decreases, the NO production ceases. The regulations make NO production by constitutively 5,6 expressed NOSs transient and short lasting . iNOS is tight even at low [Ca +]i, and therefore, iNOS is also called as a calcium-independent NOS, and it can constantly produce high levels of NO for prolonged 5,6 periods .…”

Section: Biosynthesis Of Nitric Oxidementioning

confidence: 99%

Nitric Oxide as a Target for Hypertension Management : a Review

Toma¹,

Makonnen²,

Yimer³

2014

Journal of Pharmaceutical Research

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High blood pressure is well-established as a leading cause of stroke, ischemic heart disease, and cardiovascular disease. Globally cardiovascular disease accounts for approximately 17 million deaths a year, nearly one third of the total. A number of pharmaceutical agents are available for initial treatment of high BP. These include older molecules such as diuretics and beta-blocking agents, and newer molecules such as dihydropyridine calcium channel blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and direct acting vasodilators. Comprehensive hypertension management focuses on reducing overall cardiovascular risk and should be the preferred approach for initial management of hypertension.Nitric oxide is a gaseous signaling molecule that regulates various physiological and pathophysiological responses in the human body. Nitric oxide is a gaseous lipophilic free radical which reacts with various molecules to cause pleiotropic effects and it is generated by three distinct isoforms of nitric oxide synthase. The physiologic effects include circulation and blood pressure, platelet function, host defense, and neurotransmission in central nervous system and in peripheral nerves.The etiology of the association between impaired nitric oxide bioactivity and hypertension is complex, however, and has not been fully elucidated. Important mechanisms of hypertension and cardiovascular disease, in which impaired nitric oxide bioactivity plays a major role, include arterial stiffness and increased systolic pulse wave velocity, and possibly chronic sympathetic nervous system activation to be investigated in-depth.NO plays a vital role in a wide variety of pathophysiological and biochemical reactions. Nitric oxide is a critically important mediator in the pathophysiology of different cardiac diseases. Nitric oxide has been identied as one of the key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with complications of hypertension and other cardiovascular disorders.

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Cardiovascular Effects of Peroxynitrite

Cited by 41 publications

References 53 publications

Endothelial Dysfunction Caused by Circulating Microparticles from Patients with Metabolic Syndrome

Endothelial Dysfunction Caused by Circulating Microparticles from Patients with Metabolic Syndrome

Glutathione concentration, glutathione peroxidase and glutathione reductase activity in elderly patients with type II diabetes compared to hypertensives

Nitric Oxide as a Target for Hypertension Management : a Review

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