Vascular endothelial dysfunction and pharmacological treatment
#MMPMID26635921
Su JB
World J Cardiol
2015[Nov]; 7
(11
): 719-41
PMID26635921
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The endothelium exerts multiple actions involving regulation of vascular
permeability and tone, coagulation and fibrinolysis, inflammatory and
immunological reactions and cell growth. Alterations of one or more such actions
may cause vascular endothelial dysfunction. Different risk factors such as
hypercholesterolemia, homocystinemia, hyperglycemia, hypertension, smoking,
inflammation, and aging contribute to the development of endothelial dysfunction.
Mechanisms underlying endothelial dysfunction are multiple, including impaired
endothelium-derived vasodilators, enhanced endothelium-derived vasoconstrictors,
over production of reactive oxygen species and reactive nitrogen species,
activation of inflammatory and immune reactions, and imbalance of coagulation and
fibrinolysis. Endothelial dysfunction occurs in many cardiovascular diseases,
which involves different mechanisms, depending on specific risk factors affecting
the disease. Among these mechanisms, a reduction in nitric oxide (NO)
bioavailability plays a central role in the development of endothelial
dysfunction because NO exerts diverse physiological actions, including
vasodilation, anti-inflammation, antiplatelet, antiproliferation and
antimigration. Experimental and clinical studies have demonstrated that a variety
of currently used or investigational drugs, such as angiotensin-converting enzyme
inhibitors, angiotensin AT1 receptors blockers, angiotensin-(1-7), antioxidants,
beta-blockers, calcium channel blockers, endothelial NO synthase enhancers,
phosphodiesterase 5 inhibitors, sphingosine-1-phosphate and statins, exert
endothelial protective effects. Due to the difference in mechanisms of action,
these drugs need to be used according to specific mechanisms underlying
endothelial dysfunction of the disease.
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