Dietary sodium and oxidative stress impair cutaneous microvascular function independent of blood pressure

摘要

Cardiometabolic disease is a growing public health burden and results in a number of negative physiological consequences, and there are several modifiable risk factors for cardiometabolic diseases that negatively affect the vasculature. For example, high-sodium diets, which are a risk factor for hypertension, are detrimental to endothelial function such that nitric oxide (NO)-dependent vasodilation is reduced (1, 2, 4, 8). Data demonstrating that cardiometabolic risk factors attenuate NO-dependent vasodilation in humans in vivo largely stem from studies in conduit vessels. While there is some data in the microvasculature, our composite knowledge of how disease and disease risk factors affect in vivo human microvascular NO-dependent vasodilation is much more limited.