Is vitamin C a booster of the effects of dietary nitrate on endothelial function? Physiologic rationale and implications for research
Eazaz Lbban, Ammar W. Ashor, Oliver M. Shannon, Iskandar Idris, Mario Siervo
Abstract
Endothelial dysfunction (ED) is an early marker of vascular damage linked to the loss of integrity of the endothelial lining and represents a key step in the pathogenesis of atherosclerosis and cardiovascular diseases (CVDs). ED may be reversible, hence the development and testing of effective early interventions could be beneficial for the prevention and treatment of CVDs. Recent studies have demonstrated that the consumption of dietary nitrate (NO3−), an inorganic anion which serves as a substrate for the gas transmitter nitric oxide (NO), can lower blood pressure, improve endothelial function and, in observational studies, reduce risk of CVD. We hypothesize that the co-consumption of NO3− with vitamin C, which is a potent antioxidant, could enhance the ‘yield’ of NO produced from a given NO3− dose by i) promoting a more efficient conversion between nitrite (NO2−) and NO, ii) potentiating the L-arginine pathway to increase NO generation, and iii) attenuating NO degradation. This could translate into greater NO-dependent effects on endothelial function (EF) and overall vascular health (than may be experienced with NO3− supplementation alone). This paper presents evidence to suggest that the combination of vitamin C and dietary nitrate could represent a promising and effective approach to improve EF and reduce CVDs risk, and discuss opportunities for future research.