S-nitrosothiols do not induce oxidative stress, contrary to other nitric oxide donors, in cultures of vascular endothelial or smooth muscle cells

Jaworski, Kathy; Kinard, Fabienne; Goldstein, Dan; Holvoet, Paul; Trouet, André; Schneider, Yves‐Jacques; Remacle, Claude

doi:10.1016/s0014-2999(01)01166-9

Cited by 20 publications

(11 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…20 Initial small clinical studies suggest that they may be of benefit in a variety of cardiovascular disorders. 21 S-Nitrosothiols are a class of NO-donating compounds that are naturally occurring and spontaneously release NO ϩ ; they may also gain access to the intracellular compartment by the catalytic action of plasma membranebound protein disulfide isomerase and associated transnitrosation reactions.…”

Section: Direct Donorsmentioning

confidence: 99%

Nitric Oxide Donors and Cardiovascular Agents Modulating the Bioactivity of Nitric Oxide

Ignarro

Napoli

Loscalzo

2002

Circulation Research

439

335

View full text Add to dashboard Cite

Abstract-Nitric oxide (NO) mediates multiple physiological and pathophysiological processes in the cardiovascular system. Pharmacological compounds that release NO have been useful tools for evaluating the pivotal role of NO in cardiovascular physiology and therapeutics. These agents constitute two broad classes of compounds, those that release NO or one of its redox congeners spontaneously and those that require enzymatic metabolism to generate NO. In addition, several commonly used cardiovascular drugs exert their beneficial action, in part, by modulating the NO pathway. Here, we review these classes of agents, summarizing their fundamental chemistry and pharmacology, and provide an overview of their cardiovascular mechanisms of action. ysfunction of the normally protective endothelium is found in several cardiovascular diseases, including atherosclerosis, hypertension, heart failure, coronary heart disease, arterial thrombotic disorders, and stroke. [1][2][3][4][5][6] Endothelial dysfunction leads to nitric oxide (NO) deficiency, 1,6 -11 which has been implicated in the underlying pathobiology of many of these disorders (NO insufficiency states). (For a detailed overview of the role of NO in cardiovascular biology and pathobiology, the reader is referred to Loscalzo and Vita. 3 ) NO insufficiency may reflect an absolute deficit of NO (synthesis), impaired availability of bioactive NO, or enhanced NO inactivation. Whatever its biochemical basis, NO insufficiency limits NO-mediated signal transduction of normal or protective physiological processes. In light of this pathobiology, replacement or augmentation of endogenous NO by exogenously administered NO donors has provided the foundation for a broad field of pharmacotherapeutics in cardiovascular medicine.Organic nitrate and nitrite esters represent a time-honored class of NO-donating agents used in cardiovascular therapeutics since the 19th century. These agents have direct vasoactive effects that have been used to treat ischemic heart disease, heart failure, and hypertension for many years. Treatment with conventional nitrate preparations is limited by their therapeutic half-life, systemic absorption with potentially adverse hemodynamic effects, and drug tolerance. 1,6 To overcome these limitations, novel NO donors that offer selective effects, a prolonged half-life, and a reduced incidence of drug tolerance have been developed. NO donors are pharmacologically active substances that spontaneously release, or are metabolized to, NO or its redox congeners. In the present article, we review our current understanding of NO-donating compounds and of cardiovascular drugs that modulate the bioactivity of endogenously produced NO. NO DonorsBecause of the limited utility of authentic NO gas in many experimental systems and the short half-life of NO in vivo, compounds that have the capacity to release NO have been widely used as therapeutic agents and as pharmacological tools to investigate the role of NO in cardiovascular physiology and pathophysiology. Several NO do...

show abstract

Section: Direct Donorsmentioning

confidence: 99%

Nitric Oxide Donors and Cardiovascular Agents Modulating the Bioactivity of Nitric Oxide

Ignarro

Napoli

Loscalzo

2002

Circulation Research

439

335

View full text Add to dashboard Cite

show abstract

“…Among the compounds that present high potential as The exogenous RSNOs are promising drugs to be used in the treatment of diseases that involve dysfunctions in the • NO bioavailability, as they offer advantages on the currently used drugs, due to the fact that they do not induce to tolerance in vascular cells 73 , as do the organic nitrate and sodium nitroprussiate.…”

Section: Nitric Oxide Donorsmentioning

confidence: 99%

Fatores e mecanismos envolvidos na hipertrofia ventricular esquerda e o papel anti-hipertrófico do óxido nítrico

Garcia¹,

Incerpi²

2008

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

SummaryThe left ventricular hypertrophy (LVH) occurs in response to the hemodynamic overload in some physiological and pathological conditions. However, it has not been completely elucidated whether the primary stimulation for the hypertrophy is the mechanical stretching of the heart, neurohumoral factors, or even the interaction of both. These factors are translated inside the cell as biochemical alterations that lead to the activation of second (cytosolic) and third (nuclear) messengers that will act in the cell nucleus, regulating transcription, and will finally determine the genic expression that induces LVH. The LVH is characterized by structural alterations due to the increase in the cardiomyocyte dimensions, the proliferation of the interstitial connective tissue and the rarefaction of the coronary microcirculation. Recently, nitric oxide (• NO) has appeared as an important regulator of cardiac remodeling, specifically recognized as an anti-hypertrophic mediator. Some studies have demonstrated the cellular targets, the anti-hypertrophic signaling pathways and the functional role of• NO. Thus, the LVH seems to develop as a result of the loss of the balance between the pro and the antihypertrophic signaling pathways. This new knowledge about the pro and anti-hypertrophic signaling pathways will allow the development of new strategies in the treatment of pathological LVH.

show abstract

“…Although pharmacological tolerance limits the long-term usefulness of organic nitrates, this has not been shown to be a problem for other classes of NO donors [24], including the S-nitrosothiol NO donors that are used in these studies. In addition, unlike organic nitrates and sodium nitroprusside, S-nitrosothiols have been shown to induce very limited oxidative stress [25].…”

Section: Introductionmentioning

confidence: 99%

Localized delivery of nitric oxide from hydrogels inhibits neointima formation in a rat carotid balloon injury model

Lipke

West

2005

Acta Biomaterialia

View full text Add to dashboard Cite

S-nitrosothiols do not induce oxidative stress, contrary to other nitric oxide donors, in cultures of vascular endothelial or smooth muscle cells

Cited by 20 publications

References 41 publications

Nitric Oxide Donors and Cardiovascular Agents Modulating the Bioactivity of Nitric Oxide

Nitric Oxide Donors and Cardiovascular Agents Modulating the Bioactivity of Nitric Oxide

Fatores e mecanismos envolvidos na hipertrofia ventricular esquerda e o papel anti-hipertrófico do óxido nítrico

Localized delivery of nitric oxide from hydrogels inhibits neointima formation in a rat carotid balloon injury model

Contact Info

Product

Resources

About