Magnesium infusion improves endothelium-dependent vasodilation in the human forearm

Abstract

The effect of intra-arterial magnesium infusion on endothelium-dependent vasodilation (EDV) in the forearm was studied in nine young healthy students (four men and five women). The EDV was assessed as forearm blood flow (FBF), measured by venous occlusion plethysmography, during infusion of methacholine (MCh). Endothelium-independent vasodilation (EIDV) was defined as FBF during infusion of sodium nitroprusside (SNP). During magnesium infusion in the brachial artery, 0.066 mmol/min, the concentration of ionized magnesium in venous plasma in the infused arm increased by 114%, from 0.59 (SD 0.04) to 1.26 (0.34) mmol/L (P = .0002). The FBF at baseline (ie, before administration of MCh or SNP) increased from 3.5 (1.1) to 7.3 (3.4) mL/min/100 mL tissue during magnesium infusion (P = .002). During low-dose MCh administration (2 microg/min), FBF increased by 24%, from 15.4 (5.5) to 19.1 (6.8) mL/min/100 mL tissue (P = .04), and during high-dose MCh administration (4 microg/min) FBF increased by 18%, from 20.3 (6.4) to 24.0 (7.2) mL/min/100 mL tissue (P = .04). The EIDV did not change significantly. Systemic blood pressure was not significantly altered by magnesium infusion. No change in FBF either at rest or during infusion of MCh or SNP was observed during the time-control protocol. In conclusion, this in vivo study showed that intraarterial magnesium infusion increased EDV in the infused human forearm, which is in accordance with findings in previous in vitro and animal experiments.

Regulation of the novel Mg2+ transporter transient receptor potential melastatin 7 (TRPM7) cation channel by bradykinin in vascular smooth muscle cells

“…Because of the importance of bradykinin in vascular regulation [47][48][49][50][51] and as it has been shown to regulate TRPM7 in cell lines [22,37], we questioned whether bradykinin influences TRPM7 and its downstream target annexin-1 in VSMCs. In endothelial cells, bradykinin induces dilation through nitric oxide, prostacyclin and endothelial-derived hyperpolarizing factor (EDHF), and in VSMCs it stimulates contraction, inflammation and migration through cAMP-dependent and Ca 2þ -dependent signaling pathways [47][48][49][50][51].…”

Serum magnesium in pregnancy induced hypertension

“…It synthesizes vasodilators like prostacyclins & nitric oxide thus regulates vascular tone & reactivity thereby maintains normal blood pressure. 4 Also the action of magnesium as a calcium channel blocker may a help to reduce the release of calcium and thus reducing vascular resistance. In addition, magnesium also activates the Na-K ATPase pump that controls the balance of these minerals contributing to the homeostasis of electrolytes in cells.…”

Magnesium: Effect on ocular health as a calcium channel antagonist

“…Magnesium therapy may also improve endothelial function [12,13]. In addition to reverse interaction with ET-1, magnesium induces endothelium-dependent vasodilation mediated by endothelial NO [9,10]. NO, derived from nitric oxide synthase-3 in vascular endothelium, contributes to regulation of local circulatory disturbances, and may be neuroprotective by causing vasodilation and increased blood flow in the glaucoma patients [59,60].…”

“…Elevated magnesium levels prevents ET-1 induced contractile responses by inhibition of ET-1's production and its hypertrophic effect [7,8]. Endothelium-dependent vasodilation mediated by NO is induced with magnesium by modifying formation and release of NO [9][10][11]. Indeed, magnesium therapy may improve endothelial function in patients with diabetes and coronary artery diseases [12,13].…”

“…Indeed, magnesium therapy may improve endothelial function in patients with diabetes and coronary artery diseases [12,13]. Magnesium tends to increase blood flow, and decreases vascular resistance in various vascular beds [6,9,12,14]. Hence magnesium has been shown to inhibit vasospasm in subarachnoid hemorrhages [15] and also induces vasodilation in pre-eclampsia clinically [16].…”