Nitric oxide in vascular biology

  title={Nitric oxide in vascular biology},
  author={Geoffrey A. Walford and Joseph Loscalzo},
  journal={Journal of Thrombosis and Haemostasis},
Summary.  Nitric oxide is a highly versatile heterodiatomic molecule that effects a variety of actions in the vasculture. Originally identified as a principal determination of vascular tone, nitric oxide has since been recognized to exert anti thrombotic, antiproliferative, and anti‐inflammatory effects in the vasculture. At higher concentrations and in the setting of other oxidants, nitric oxide can promote vascular pathology. In this review, we summarize the molecular mechanisms of nitric… 

Nitric oxide insufficiency and atherothrombosis

An overview of NO synthesis and biological chemistry is presented, the mechanisms of action of NO in regulating endothelial and platelet function are discussed, and the causes of NO insufficiency are explored, as well as the evidence linking these causes to the pathophysiology of endothelial dysfunction and atherothrombosis.

Role of oxidative stress and nitric oxide in atherothrombosis.

This review examines the role of oxidative stress and NO in mechanisms of endothelial and vascular dysfunction with an emphasis on atherothrombosis.

The potential of stimulating nitric oxide formation in the treatment of hypertension

There is now evidence supporting the notion that many cardiovascular drugs activate NO signaling or enhance NO bioavailability as a contributing mechanism to their beneficial cardiovascular effects.

Effect of nitric oxide reduction on arterial thrombosis

Network medicine is an emerging paradigm that ideally overcomes the current shortcomings of the reductionist approach and might reveal the key nodes underlying the perturbations of the arterial thrombosis, thus advancing personalized therapy.

Nitric oxide release: part I. Macromolecular scaffolds.

An overview of the most promising NO release scaffolds including protein, organic, inorganic, and hybrid organic-inorganic systems are provided, chosen based on their enhanced NO storage, tunable NO release characteristics, and potential as therapeutics.

Nox and Inflammation in the Vascular Adventitia.

This review-based update acts as a springboard for a revitalized debate of the adventitia’s role in vascular disease, addressing the role of adventitial Nox-derived ROS from a perivascular viewpoint looking inwards to promoting vascular inflammation and disease.



Inducible nitric oxide synthase and vascular injury.

Biochemistry of nitric oxide and its redox-activated forms.

The integration of this chemistry with current perspectives of NO biology illuminates many aspects of NO biochemistry, including the enzymatic mechanism of synthesis, the mode of transport and targeting in biological systems, the means by which its toxicity is mitigated, and the function-regulating interaction with target proteins.

Nitric oxide as a secretory product of mammalian cells

How different forms of nitric oxide synthase help confer specificity and diversity on the effects of this remarkable signaling molecule is reviewed.

Nitric oxide as a bioregulator of apoptosis.

The antiapoptotic mechanism can be understood via expression of protective genes such as heat shock proteins, Bcl-2 as well as direct inhibition of the apoptotic caspase family proteases by S-nitrosylation of the cysteine thiol.

Hypertension in mice lacking the gene for endothelial nitric oxide synthase

Responses to NOS blockade in the mutant mice suggest that non-endothelial isoforms of NOS may be involved in maintaining blood pressure, and eNOS mediates basal vasodilation.

Interactions Between Nitric Oxide and Lipid Oxidation Pathways: Implications for Vascular Disease

The biochemical interactions between ·NO and lipid oxidation reactions are summarized and the recognized and potential roles of these reactions in the vasculature are discussed.

Inducible nitric oxide: an autoregulatory feedback inhibitor of vascular inflammation.

These studies indicate that iNO attenuates iNOS expression in macrophages and inhibits monocyte adhesion to endothelial cells, and suggest that endogenously derived iNO may be an important autoregulatory inhibitor of vascular inflammation.