Effect of chronic stress and sleep deprivation on both flow-mediated dilation in the brachial artery and the intracellular magnesium level in humans.

Abstract

Chronic mental and physical stress has been suggested to be a trigger for cardiovascular events. In addition, a reduction in levels of intracellular magnesium has been reported to cause vasoconstriction while enhancing platelet-dependent thrombosis. The purpose of this study was to investigate whether chronic stress affects endothelial function and intracellular magnesium levels in humans. Flow-mediated dilation (endothelium-dependent vasodilation) and sublingual nitroglycerin-induced dilation (0.3 mg, endothelium-independent vasodilation) were measured in the brachial artery in 30 healthy male college students, aged 22 +/- 1 years, using high-resolution ultrasound both before and immediately after a 4-week final term examination period. Erythrocyte magnesium concentration was measured simultaneously. All students had chronic sleep deprivation for 4 weeks, during which sleep lasted < 80% of that on ordinary days; in addition, the students were under great stress to pass the examination. This condition was considered to be chronic stress. Chronic stress decreased flow-mediated dilation and erythrocyte magnesium concentration (from 7.4 +/- 3.0 to 3.7 +/- 2.3%, p < 0.05; from 5.7 +/- 0.4 to 5.5 +/- 0.4 mg/ml, p < 0.05, respectively). The change in flow-mediated dilation correlated significantly with that of the erythrocyte magnesium concentration (r = 0.43, p < 0.05), but not with nitroglycerin-induced dilation. Chronic stress was found to attenuate endothelial function, which may also be associated with a reduction in the intracellular magnesium level in humans.