The role of acute phosphate supplementation in endothelium-dependent and -independent vasodilation

Abstract

Phosphate is a mineral component of the human diet that is essential for life. However, elevated blood phosphate levels are associated with cardiovascular disease and death in the general population. The mechanisms through which phosphate may be detrimental to cardiovascular health remain unclear, however there is emerging evidence that suggests phosphate may impair the function of human arteries. The purpose of this study was to investigate whether a single phosphate supplement affects the ability of the brachial artery to dilate in response to: a) increases in blood flow (flow-mediated dilation, FMD), b) a drug that causes dilation (GTN), or c) both FMD and GTN. 17 healthy male participants (22.9 ±3.07 years old) were exposed to phosphate (PHOS) and placebo (PLAC) conditions over two experimental days (one each visit) in a within-subjects, randomized, double-blinded, placebo-controlled trial. Subjects drank a liquid containing 1200 mg of phosphorus or a placebo. FMD tests were performed pre- and 20 min, 60 min and 120 min post-supplement or placebo ingestion by a standard procedure involving the occlusion of blood flow to the forearm (reactive hyperemia). Blood phosphate concentrations were significantly greater in PHOS vs. PLAC, but did not increase differently between the two groups. Blood phosphate concentrations were significantly greater 60 min vs. 20 min post-supplement in both conditions. Phosphate excretion increased 315% in the PHOS vs. PLAC condition, indicating that the kidney rapidly removed phosphate from the blood. There was no difference in FMD between PHOS and PLAC conditions at any post-supplement time point. There was no effect of PHOS on the GTN tests. These findings indicate that a single phosphate supplement did not impair brachial artery dilation in response to increases in blood flow or the administration of a drug that induces dilation. Also, the phosphate supplement did not substantially increase phosphate concentrations in the blood likely due to a large excretion of phosphate by the kidneys. Further research is needed to better understand how phosphate may be linked to vascular function.