| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
intracellular ATP level. Especially, in ischemic myocardium, K ATP channel is known to be one of the most important component, and several other channels which are modulated by intracellular ATP level. are also contributing by determining. action potential duration. We analyzed the function of these channel... by patch-clump method in cultured cells which overexpressing KCNQ1, the subunit of delayed rectifier K channel. Analyses using tyrosin kinase, ATP analogue, or phosphatidylinositol 4.5-bisghoshpate revealed that this channel protein has direct effects on cell swelling induced enhancement of slowly activating delayed rectifier K current. It is imortant to analyze the relationship between cell swelling in myocardial damage and KCNQ1 function In clinical medicine, acute myocardial infarction is frequently acompanies fatal dysrhythmias. QT prolongation, ECG change during exercise, and modulation by several drugs are most critical determinants of these dysrhythmias. Hereditary long QT syndrome is a nice model to analyze these factors. K channel anomalies (LQT1 and LQT2) are closely related with specific ECG changes during exercise, and has a possible profound significance to predict sudden death. We found a new mutation in SCN5A sodium channel protein, L1855A, and that induces sodium peak current reduction, and cusses lethal arrhythmia in bradycardia and drug challenge. We also discovered the mechanism how mutation at PIP binding site in KCNJ2 channel expressed dominant negative effect, and caused arrhythmia in patients with Anderson syndrome. To investigate how these disorders in ion channel affect ischemic myocardium causing dysrhythmia is one of the most challenging field
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