Identification and quantitative analysis of the cell membrane MgィイD1[2+]ィエD1 transporter in cardiac and smooth muscles.

A fluorescent Mg - D12+ D1 indicator, furaptra (mag-fura-2)，was loaded into smooth muscle cells of guinea-pig tenia cecum，and cytoplasmic Mg - D12+ - D1 concentration ([Mg - D12+ - D1] - D2i - D2) was measured. Loweringextracellular Na - id1 + id1 concentration ([Na - id1 + id1] D2o - id2)in the absence of Ca - id12 + id1caused gradual elevation of [Mg - D12+ d - D1] d - 2i - D2,the rate was strongly dependent on[Na - D2o - D2 with the maximal rate of rise of 0.16μM./ s.b we also measured[Mg D12+ D1] Mg D2i - D2 in rat ventricular myocytes. [Mg D12+ D1] Mg D2i - D2 was elevated when cellswere treated with ionomycin in 10mm extracellular Mg - D12+ d - 1([Mg - D12+ d - 1] - D2o - 2). The ratof rise of [Mg D12+ die D1] die D2i die D2 was reduced in the higher [Na die D1+ die D1] die D2o die D2. the net effluxMg D12+ D1 from the loaded cells was also markedly inhibited by the presence of 140mmNa - D1+ D1. these results suggest the exixtence of the Na - D1+ D1-dependent Mg - D12+ D1 transport（Na - D1+ D1- mg + D12+ D1 exchange） in smooth muscle and cardiac muscle cells. The rate ofMg - D12+ - D1 transport was estimated to be 0.026 pmol/cm - D12 - D12 - s in tenia and 0.085pmol/cm d - 12 d - 1 s in cardiac myocytes at 25℃. It is unlikely that the Na d - 1+ d - 1- ca d - 12+ d - 1exchanger is mainly responsible for this Mg D12+ D1 transport，because only the slight Na - D1+ D1- mg - D12+ D1 exchange activity was observed in the CCL39 cellsoverexpressing the Na - D1+ D1- ca - D12+ D1 exchanger。

A fluorescent MgィイD12+ィエD1 indicator, furaptra (mag-fura-2), was loaded into smooth muscle cells of guinea-pig tenia cecum, and cytoplasmic MgィイD12+ィエD1 concentration ([MgィイD12+ィエD1]ィイD2iィエD2) was measured. Lowering extracellular NaィイD1+ィエD1 concentration ([NaィイD1+ィエD1]ィイD2oィエD2)in the absence of CaィイD12+ィエD1 caused gradual elevation of [MgィイD12+ィエD1]ィイD2iィエD2,the rate was strongly dependent on [NaィイD1+ィエD1]ィイD2oィエD2 with the maximal rate of rise of 0.16μM./s.We also measured [MgィイD12+ィエD1]ィイD2iィエD2 in rat ventricular myocytes. [MgィイD12+ィエD1]ィイD2iィエD2 was elevated when cells were treated with ionomycin in 10 mM extracellular MgィイD12+ィエD1([MgィイD12+ィエD1]ィイD2oィエD2). The rat of rise of [MgィイD12+ィエD1]ィイD2iィエD2 was reduced in the higher [NaィイD1+ィエD1]ィイD2oィエD2. The net efflux of MgィイD12+ィエD1 from the loaded cells was also markedly inhibited by the presence of 140 mM NaィイD1+ィエD1.These results suggest the exixtence of the NaィイD1+ィエD1-dependent MgィイD12+ィエD1 transport (NaィイD1+ィエD1-MgィイD12+ィエD1 exchange) in smooth muscle and cardiac muscle cells. The rate of MgィイD12+ィエD1 transport was estimated to be 0.026 pmol/cmィイD12ィエD1・s in tenia and 0.085 pmol/cmィイD12ィエD1・ s in cardiac myocytes at 25℃. It is unlikely that the NaィイD1+ィエD1-CaィイD12+ィエD1 exchanger is mainly responsible for this MgィイD12+ィエD1 transport, because only the slight NaィイD1+ィエD1-MgィイD12+ィエD1 exchange activity was observed in the CCL39 cells overexpressing the NaィイD1+ィエD1-CaィイD12+ィエD1 exchanger.