| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Research Abstract |
It has been reported that Prinzmetal-type angina pectoris is observed in Kir6.2-deficient or SUR2-deficient mice. In order to determine whether dysfunction of ATP-sensitive K^+ (KATP) channels in endothelial cells is involved in the development of vasospastic angina in Kir6.2-deficient or SUR2-deficient mice, we evaluated elecrophysiological responses to K^+ channel openers by using patch clamp techniques and gene expression by using real time PCR in endothelial cells. K^+ channel openers failed to affect the membrane potentials in vascular endothelial cells isolated from pulmonary tissues of wild type mouse and cultured mouse endothelial cells (UV cells). Ion channel genes related to KATP channels were hardly detected in these endothelial cells. In contrast, in mouse urinary bladder mRNA of Kir6.1 and SUR2B could be detected by RT-PCR. The K^+ channel opener pinacidil induced KATP current in visceral smooth muscle cells of wild type and Kir6.2-deficient mice, but not those of Kir6.1-deficient mice. These results suggest that KATP channel in vascular endothelial cells is unlikely to play an important role in the induction of vasospastic angina in mouse.
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