Free radical production by dysfunctional eNOS

Marianne C. Verhaar

doi:10.1136/hrt.2003.029405

April 14, 2004HeartOpen Access

Free radical production by dysfunctional eNOS

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Key Points

To review the mechanisms through which endothelial nitric oxide synthase becomes dysfunctional and produces free radicals, driving cardiovascular disease pathogenesis.
Synthesized molecular and physiological evidence from genetic knockout and pharmacological inhibition animal models of endothelial nitric oxide synthase.
Assessed clinical observations connecting established cardiovascular risk factors to endothelial dysfunction and impaired nitric oxide bioavailability.
Inhibition or genetic deletion of eNOS in animal models induces hypertension, vascular thrombosis, abnormal vascular remodeling, and accelerated atherogenesis.
Human cardiovascular risk factors impair nitric oxide bioavailability via oxidative degradation into peroxynitrite by superoxide anions, and such endothelial impairment independently predicts adverse cardiac events.

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Endothelial dysfunction characterized by impaired nitric oxide bioavailability is a key mechanism linking cardiovascular risk factors to adverse cardiac events.

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Cite This Study

Marianne C. Verhaar (2004) studied this question.

synapsesocial.com/papers/6a8379176524aee222604c68 https://doi.org/10.1136/hrt.2003.029405

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Free radical production by dysfunctional eNOS

Key Points

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Implication

Abstract

Discussion

Cite This Study

Free radical production by dysfunctional eNOS

Key Points

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Implication

Abstract

Discussion

Cite This Study

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