Editing Endothelial dysfunction (section)

===Nitric oxide===
Nitric oxide (NO) suppresses platelet aggregation, inflammation, oxidative stress, vascular smooth muscle cell migration and proliferation, and leukocyte adhesion.<ref name="pmid24222847" /> A feature of endothelial dysfunction is the inability of [[arteries]] and [[arterioles]] to dilate fully in response to an appropriate stimulus, such as [[exogenous]] [[nitroglycerine]],<ref name=jh/> that stimulates release of [[Vasodilation|vasodilators]] from the endothelium like NO. Endothelial dysfunction is commonly associated with decreased NO bioavailability, which is due to impaired NO production by the endothelium or inactivation of NO by reactive [[oxygen]] species.<ref name="pmid25804383">{{cite journal | vauthors = Gradinaru D, Borsa C, Prada GI | title=Oxidized LDL and NO synthesis--Biomarkers of endothelial dysfunction and ageing | journal= Mechanisms of Ageing and Development | volume=151 | pages=101–113 | year=2015 | doi= 10.1016/j.mad.2015.03.003 | pmid=25804383| doi-access=free }}</ref><ref name="pmid29596860">{{cite journal | vauthors = Yuyun MF, Ng LL, Ng GA | title=Endothelial dysfunction, endothelial nitric oxide bioavailability, tetrahydrobiopterin, and 5-methyltetrahydrofolate in cardiovascular disease. Where are we with therapy? | journal= Microvascular Research | volume=119 | pages=7–12 | year=2018 | doi= 10.1016/j.mvr.2018.03.012 | pmid=29596860}}</ref> As a co-factor for [[nitric oxide synthase]], [[tetrahydrobiopterin]] (BH4) supplementation has shown beneficial results for the treatment of endothelial dysfunction in animal experiments and clinical trials, although the tendency of BH4 to become oxidized to BH2 remains a problem.<ref name="pmid29596860" />