The Protective Role of Vitamin C on Endothelial Dysfunction

A major function of endothelium is the secretory control of smooth muscle vascular tone. The principal vasodilator substance excreted is nitric oxide (NO), a molecule that is under thorough investigation. There is sufficient evidence that its bioavailability is reduced in many diseases such as coronary artery disease, heart failure, dyslipidaemias, obesity, diabetes, renal failure, and others. The interactions of this molecule with reactive oxygen species are believed to constitute an important pathophysiological pathway. Consequently, intensive research is under way to evaluate the efficacy of various antioxidant interventions against endothelial dysfunction. Vitamin C is an outstanding hydrophilic antioxidant, which is able to scavenge many reactive oxygen species. When infused or chronically ingested in pharmacological doses it substantially improves the defective endothelium-dependent vasodilation involved in the above-mentioned clinical conditions. Several molecular mechanisms have been proposed for this protective effect including scavenging of superoxide anion, inhibition of LDL-oxidation, inhibition of inflammatory cell adhesion, stabilization of NO-synthase through reduction of tetrahydrobiopterin, NO-release from plasma nitrosothiols and preservation of guanyl cyclase activity. Although the experimental evidence is promising, further human clinical trials are necessary before preventive and therapeutic interventions using vitamin C become an established clinical practice. J Clin Basic Cardiol 2003; 6: 3–6.