A vascular smooth muscles nitric oxide relaxation by a mechanism distinct of calcium changes

Chabaud, Fabienne; Danna, Mireille; Bény, Jean‐Louis

doi:10.1016/0024-3205(94)00600-8

Cited by 6 publications

(2 citation statements)

References 20 publications

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“…The stability of NO is lower than other powerful endothelial vasodilators such as prostacyclin, which together with NO causes platelet antiaggregation and vasorelaxation effects by different mechanism [41]. NO is known to readily bind certain transition metal ions and many of its physiological effects are exerted as a result of its initial binding to Fe 2+ haem groups in the enzyme guanylate cyclase.…”

Section: Mechanism Of Nitric Oxide Actionmentioning

confidence: 99%

Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

Tuteja

Chandra

Tuteja

et al. 2004

BioMed Research International

196

128

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Nitric oxide (NO) is an intra- and extracellular messenger that mediates diverse signaling pathways in target cells and is known to play an important role in many physiological processes including neuronal signaling, immune response, inflammatory response, modulation of ion channels, phagocytic defense mechanism, penile erection, and cardiovascular homeostasis and its decompensation in atherogenesis. Recent studies have also revealed a role for NO as signaling molecule in plant, as it activates various defense genes and acts as developmental regulator. In plants, NO can also be produced by nitrate reductase. NO can operate through posttranslational modification of proteins (nitrosylation). NO is also a causative agent in various pathophysiological abnormalities. One of the very important systems, the cardiovascular system, is affected by NO production, as this bioactive molecule is involved in the regulation of cardiovascular motor tone, modulation of myocardial contractivity, control of cell proliferation, and inhibition of platelet activation, aggregation, and adhesion. The prime source of NO in the cardiovascular system is endothelial NO synthase, which is tightly regulated with respect to activity and localization. The inhibition of chronic NO synthesis leads to neurogenic and arterial hypertensions, which later contribute to development of myocardial fibrosis. Overall, the modulation of NO synthesis is associated with hypertension. This review briefly describes the physiology of NO, its synthesis, catabolism, and targeting, the mechanism of NO action, and the pharmacological role of NO with special reference to its essential role in hypertension.

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Section: Mechanism Of Nitric Oxide Actionmentioning

confidence: 99%

Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

Tuteja

Chandra

Tuteja

et al. 2004

BioMed Research International

196

128

View full text Add to dashboard Cite

show abstract

“…Mouse and human peripheral blood leukocytes were incubated with M. bovis BCG or L. monocytogenes in the presence of fluorochrome di-hydrorhodamine 123. Upon oxidation, di-hydro-rhodamine 123 turns into the fluorescent mono-hydro-rhodamine as a measurement for the production of reactive oxygen and nitrogen intermediates [38][39][40][41][42][43][44]. As shown in figure 7, mouse and, more evidently, human neutrophils exhibited considerably less fluorescent mono-hydro-rhodamine after phagocytosis of M. bovis BCG than after phagocytosis of L. monocytogenes, indicating less production of reactive oxygen and nitrogen intermediates after infection by M. bovis BCG.…”

Section: Specific Depletion Of Neutrophils By Treatment With Mab Rb6-mentioning

confidence: 99%

Rapid Neutrophil Response Controls Fast‐Replicating Intracellular Bacteria but Not Slow‐ReplicatingMycobacterium tuberculosis

et al. 2000

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Being one of the first cells to invade the site of infection, neutrophils play an important role in the control of various bacterial and viral infections. In the present work, the contribution of neutrophils to the control of infection with different intracellular bacteria was investigated. Mice were treated with the neutrophil-depleting monoclonal antibody RB6-8C5, and the time course of infection in treated and untreated mice was compared by using intracellular bacterial species and strains varying in virulence and replication rate. The results indicate that neutrophils are crucial for the control of fast-replicating intracellular bacteria, whereas early neutrophil effector mechanisms are dispensable for the control of the slow-replicating Mycobacterium tuberculosis.

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Introduction to Free Radicals, Antioxidants, Lipid Peroxidation, and Their Effects on Cell Proliferation

Das¹

2020

Molecular Biochemical Aspects of Cancer

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A vascular smooth muscles nitric oxide relaxation by a mechanism distinct of calcium changes

Cited by 6 publications

References 20 publications

Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

Rapid Neutrophil Response Controls Fast‐Replicating Intracellular Bacteria but Not Slow‐ReplicatingMycobacterium tuberculosis

Introduction to Free Radicals, Antioxidants, Lipid Peroxidation, and Their Effects on Cell Proliferation

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