Project/Area Number |
09670055
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Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General physiology
|
Research Institution | Tokyo Medical University (1999) Jikei University School of Medicine (1997-1998) |
Principal Investigator |
KONISHI Masato Tokyo Medical University, Department of Physiology, Professor, 医学部, 教授 (20138746)
|
Co-Investigator(Kenkyū-buntansha) |
HONGO Kenichi The Jikei University School of Medicine, Department of Medicine, Lecturer, 医学部, 講師 (00256447)
|
Project Period (FY) |
1997 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
Keywords | Magnesium / Sodium / Transporter / Smooth muscle / Cardiac muscle / NaィイD1+ィエD1-CaィイD12+ィエD1 exchange / NaィイD1+ィエD1-MgィイD12+ィエD1 exchange / antiport / 細胞内Mg濃度 / 細胞内Ca濃度 / Na-Ca交換輸送 / 蛍光Mg指示薬 / モルモット / 盲腸紐 / 平滑筋細胞 / 細胞内Na濃度 / Na-Mg交換輸送 |
Research Abstract |
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.
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