Affiliations: University of Western Australia School of Medicine and
Pharmacology and the Western Australian Institute for Medical Research, Royal
Perth Hospital, Western Australia, Australia
Note: [] Address for correspondence: A/Professor Gerald Watts, School of
Medicine & Pharmacology, GPO Box X2213, Perth, WA 6847, Australia. Tel.:
+61 8 9224 0248; Fax: +61 8 9224 0246; E-mail: gfwatts@cyllene.uwa.edu.au
Abstract: Coenzyme Q_{10} (CoQ) is an endogenously
synthesised compound that acts as an electron carrier in the mitochondrial
electron transport chain. The presence of adequate tissue concentrations of CoQ
may be important in limiting oxidative and nitrosative damage in vivo.
Oxidative and nitrosative stress are likely to be elevated in conditions such
as diabetes and hypertension. In these conditions elevated oxidative and
nitrosative stress within the arterial wall may contribute to increased blood
pressure and vascular dysfunction. The major focus of this review is the
potential of CoQ to improve vascular function and lower blood pressure.
Although there is substantial indirect support for the putative mechanism of
effect of CoQ on the vascular system, to date there is little direct support
for an effect of CoQ on in vivo markers of oxidative or nitrosative
stress. The limited data available from studies in animal models and from human
intervention studies are generally consistent with a benefit of CoQ on vascular
function and blood pressure. The observed effects of CoQ on these endpoints are
potentially important therapeutically. However, before any firm clinical
recommendations can be made about CoQ supplementation, further intervention
studies in humans are needed to investigate the effects of CoQ on vascular
function, blood pressure and cardiovascular outcomes. The particularly relevant
groups of patients for these studies are those with insulin resistance, type 2
diabetes, hypertension and the metabolic syndrome.
