Cited by 612Nitric Oxide and Endothelin EffectsPlatelet Disorders and TreatmentsBlood Coagulation and Thrombosis Mechanisms

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Nitric Oxide Insufficiency, Platelet Activation, and Arterial Thrombosis

Loscalzo, Joseph·2001·Circulation Research

DOI 10.1161/hh0801.089861

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Abstract

Abstract—Nitric oxide (NO) was originally discovered as a vasodilator product of the endothelium. Over the last 15 years, this vascular mediator has been shown to have important antiplatelet actions as well. By activating guanylyl cyclase, inhibiting phosphoinositide 3-kinase, impairing capacitative calcium influx, and inhibiting cyclooxygenase-1, endothelial NO limits platelet activation, adhesion, and aggregation. Platelets are also an important source of NO, and this platelet-derived NO pool limits recruitment of platelets to the platelet-rich thrombus. A deficiency of bioactive NO is associated with arterial thrombosis in animal models, individuals with endothelial dysfunction, and patients with a deficiency of the extracellular antioxidant enzyme glutathione peroxidase-3. This enzyme catalyzes the reduction of hydrogen and lipid peroxides, which limits the availability of these reactive oxygen species to react with and inactivate NO. The complex biochemical reactions that underlie the function and inactivation of NO in the vasculature represent an important set of targets for therapeutic intervention for the prevention and treatment of arterial thrombotic disorders.

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Authors: Loscalzo, J.
Affiliations: Boston University (US)
Corresponding author: Loscalzo, Joseph
ORCID: Loscalzo, Joseph
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2001-04-27
Volume: 88
Issue: 8
Pages: 756-762
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/hh0801.089861
OpenAlex: W2113684546
Cited by: 612
References: 80
Citations by year: 2026: 18 · 2025: 21 · 2024: 22 · 2023: 21 · 2022: 22 · 2021: 19 · 2020: 25 · 2019: 15 · 2018: 28 · 2017: 25 · 2016: 16 · 2015: 24 · 2014: 27 · 2013: 28 · 2012: 29
FWCI: 3.28
Type: journal article
Language: en
Open access: closed
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Heart, Lung, and Blood Institute (HL61795, HL 55993, HL58976, R01HL058976, P50HL055993)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Keywords: nitric oxide, platelet activation, arterial thrombosis, endothelial dysfunction, glutathione peroxidase 3, phosphatidylinositol 3-kinase, cyclooxygenase-1, guanylate cyclase, platelet aggregation, thromboprophylaxis
MeSH terms: Animals, Arteries, Blood Platelets, Endothelium, Vascular, Glutathione Peroxidase, Humans, Nitric Oxide, Thrombosis, Vasodilator Agents, Platelet Activation, Reactive Oxygen Species, Nitric Oxide Donors

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Nitric Oxide Insufficiency, Platelet Activation, and Arterial Thrombosis

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