Mg²⁺-Induced Vasodilation in Human Forearm Vasculature Is Inhibited by NG-Monomethyl- L-Arginine but Not by Indometacin

We have investigated the mechanism of the vasodilator action of Mg²⁺ in human forearm resistance vasculature. Venous occlusion plethysmography was used to measure vasodilator responses to Mg²⁺ infused via the brachial artery in healthy men, and to determine effects on Mg²⁺ responses of indometacin (an inhibitor of cyclo-oxygenase) and of NG-monomethyl-L-arginine (L-NMMA, an inhibitor of the L-arginine/nitric oxide, L-arg/NO, pathway). Magnesium sulphate infusion (0.05, 0.1, 0.2 mmol·min–¹) increased plasma Mg²⁺ concentration to 1.57 ± 0.16 mmol·l–¹ in venous blood from the infused arm at the highest dose. There was a dose-related increase in forearm blood flow in the infused arm to a maximum of 6.37 ± 1.37 ml·min–¹·dl forearm–¹ at the highest dose corresponding to an increase of 159 ± 25% in blood flow relative to the non-infused arm. There was no tachyphylaxis during a second infusion following a 21-min recovery period. Indometacin had no effect on vasodilator responses to Mg²⁺, whereas L-NMMA inhibited Mg²⁺ responses (area under the dose-response curve) by 43 ± 6% (p = 0.0003 by repeated-measures ANOVA). Therefore the L-arg/NO pathway is responsible, in part, for the vasodilator action of Mg²⁺ in human forearm resistance vasculature.