Nitric oxide dysfunction in vascular endothelium and platelets: role in essential hypertension.
Both endothelial and platelet-derived nitric oxide have important vasculoprotective properties. Increasing evidence suggests a dysfunctional platelet nitric oxide synthase type 3 (NOS3) pathway in essential hypertension, whereas for endothelial-derived nitric oxide the picture is more complicated, with many studies suggesting an impairment of endothelial nitric oxide generation, whilst others have suggested that the endothelial nitric oxide pathway is preserved. Controversy also exists as to whether any observed reduction in endothelial or platelet-derived nitric oxide exerts a pathogenetic role or is simply the result of the raised blood pressure. In this review, we examine the evidence that endothelial and/or platelet-derived nitric oxide are disturbed in essential hypertension, and whether such disturbances are cause or effect.
Department of Clinical Pharmacology, Cardiovascular Division, King's College London, London, UK.
Eugenia
E
Gkaliagkousi
Stella
S
Douma
Chrysanthos
C
Zamboulis
Albert
A
Ferro
D001792:Blood Platelets / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D004730:Endothelium, Vascular / Q000201:enzymology*; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D018384:Oxidative Stress; D014664:Vasodilation / Q000502:physiology
D009569:Nitric Oxide; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III