| Budget Amount *help |
¥3,790,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥690,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥800,000 (Direct Cost: ¥800,000)
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| Research Abstract |
Changes in the luminal NaCl concentration ([NaCl]) at the kidney macula densa (MD) modulate the tubuloglomerular feedback (TGF) responses via affecting the release of nitric oxide (NO). In a newly established mouse macula densa cell line (NE-MD), we demonstrated that furosemide, an inhibitor of Na^+-K^+-2Cl^- cotransporter, and low [Cl^-] similarly induced increases in both the nNOS protein expression and the L-Arg-induced NO generation. We also found that the nNOS-like protein (60kD) determined in the NE-MD cells was smaller in size than the usual nNOS proteins (160kD) obtained from brain and skeletal muscle. Molecular structure of the NE-MD nNOS protein was carefully analyzed by the two-dimensional electrophoresis and the mass spectrometry (MALDI-TOF-MS). Based on the observation of the MS analysis of the peptide piece, we conclude that a main part of the nNOS reduction domain has been deleted in the furosemide-induced nNOS protein of NE-MD.
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