Endothelial dysfunction and oxidative stress in arterial hypertension.
A large body of evidence indicates that endothelial dysfunction is a characteristic of patients with essential hypertension. By definition, endothelial dysfunction is a functional and reversible alteration of endothelial cells, resulting from impairment in nitric oxide (NO) availability and oxidative stress. Superoxide anion is a major determinant of NO biosynthesis and also acts as a vasoconstrictor. In addition, NO synthase (NOS) can generate superoxide rather than NO in response to atherogenic stimuli ("NOS uncoupling"). Under these circumstances, NOS may become a peroxynitrite generator, leading to a dramatic increase in oxidative stress, since peroxynitrite has additional detrimental effects on vascular function by lipid peroxidation. Increased levels of biomarkers of lipid peroxidation and oxidative stress have been found in patients with hypertension. In particular, patients with hypertension-related microvascular changes showed increased lipid peroxidation and platelet activation when compared with patients with absent or early signs of retinopathy. Furthermore, oxidant stress has been shown to play an important role in promoting a prothrombotic state in the vascular system. For all these reasons, endothelial dysfunction is evoked in hypertensive patients as promotor of vascular progressive damage and atherosclerotic and thrombotic complications through the enhanced oxidative stress of arterial walls. This broadens the cardiovascular risk of hypertensive patients and explains the insufficient role of the strict BP reduction in the prevention of vascular complications, thus opening up new perspectives on the antioxidant properties of currently available antihypertensive drugs and supplementation with antioxidant principles.
Ferroni
P
P
Department of Laboratory Medicine and Advanced Biotechnologies, IRCCS San Raffaele, Rome, Italy.
Basili
S
S
Paoletti
V
V
Davì
G
G
D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology / Q000378:metabolism; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D015227:Lipid Peroxidation; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D015539:Platelet Activation / Q000502:physiology*