Na+‐independent Mg2+ transport sensitive to 2‐aminoethoxydiphenyl borate (2‐APB) in vascular smooth muscle cells: involvement of TRPM‐like channels

Abstract

Magnesium is associated with several important cardiovascular diseases. There is an accumulating body of evidence verifying the important roles of Mg²⁺‐permeable channels. In the present study, we estimated the intracellular free Mg²⁺ concentration ([Mg²⁺]_i) using ³¹P‐nuclear magnetic resonance (³¹P‐NMR) in porcine carotid arteries. pH_i and intracellular phosphorus compounds were simultaneously monitored. Removal of extracellular divalent cations (Ca²⁺ and Mg²⁺) in the absence of Na⁺ caused a gradual decrease in [Mg²⁺]_i to ∼60% of the control value after 125 min. On the other hand, the simultaneous removal of extracellular Ca²⁺ and Na⁺ in the presence of Mg²⁺ gradually increased [Mg²⁺]_i in an extracellular Mg²⁺‐dependent manner. 2‐aminoethoxydiphenyl borate (2‐APB) attenuated both [Mg²⁺]_i load and depletion caused under Na⁺‐ and Ca²⁺‐free conditions. Neither [ATP]_i nor pH_i correlated with changes in [Mg²⁺]_i. RT‐PCR detected transcripts of both TRPM6 and TRPM7, although TRPM7 was predominant. In conclusion, the results suggest the presence of Mg²⁺‐permeable channels of TRPM family that contribute to Mg²⁺ homeostasis in vascular smooth muscle cells. The low, basal [Mg²⁺]_i level in vascular smooth muscle cells is attributable to the relatively low activity of this Mg²⁺ entry pathway.