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. pHi 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 pHi 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.