Magnesium and blood pressure: A physiology-based approach 85 4 that BP reductions might be a result of improved vascular stiffness after magnesium supplementation, rather than a cause. Alternatively, the total magnesium dose of 350 mg/d may have been too small to elicit an effect on BP. This is in agreement with a metaanalyses that found a more pronounced effect of magnesium on BP in a subgroup analysis with higher-dose supplementation (>370 mg) 16. Additional mechanisms to explain the effect of magnesium supplementation on vascular stiffness might relate to the beneficial effects of magnesium on inflammation, oxidative stress and endothelial function 44–47. Afsar and colleagues observed a relationship between serum magnesium levels and augmentation index, which is a measure for the arterial pressure waveform that depends on the tone of the peripheral resistance arteries 48. Interestingly, no association was found between magnesium levels and BP, vascular stiffness and cardiac output. These findings might not be easy to explain, given the fact that augmentation indexwas highly correlated with pulse pressure, pulse wave velocity and peripheral resistance.The authors suggested that the underlying mechanism linking magnesium and augmentation index may include VC and that VC may not affect vascular stiffness or that pulse wave velocity may not be a sensitive marker to detect such changes. However, this study might be limited due to its cross-sectional study design. Endothelial Function Hypomagnesaemia has been previously linked to the inhibition of nitric oxide release 49, which can cause increased vascular tone and subsequently high BP. Furthermore,Watson and colleagues reported that magnesium stimulated the release of prostacyclin 45. In addition, intervention studies showed that magnesium supplementation results in a significant improvement in endothelial function, measured by flow-mediated vasodilation (FMD) 44. Interestingly, the authors were also able to measure intracellular magnesium concentrations, and they observed a positive correlation with baseline FMD (r=0.48; p<0.01). A recently published clinical trial showed no effect on FMD by magnesium supplementation, nor on plasma markers for microvascular endothelial function (sVCAM-1, sICAM-1 and sE-selectin) 50. However, in this study, subjects were characterized as healthy overweight subjects with normal magnesium levels, and therefore (near-)normal endothelial function might have been more difficult to be modified by magnesium supplementation, which was given in a relatively low dose. Inflammation and oxidative stress Magnesium deficiency has been linked to inflammation in animal models 46, suggesting that this is a pathway between magnesium and total peripheral resistance. Interestingly,
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