Functional role of ATP-sensitive K^+ channel in vascular endothelial cells
| Project/Area Number |
20590249
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Chiba University |
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Principal Investigator |
NAKAYA Haruaki Chiba University, 大学院・医学研究院, 教授 (60113594)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| 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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| Keywords | 心血管 / 血液 / チャネル / K_<ATP>チャネル / 血管内皮細胞 / 血管平滑筋細胞 / 内臓平滑筋細胞 / 遺伝子欠損動物 / 冠動脈攣縮 / 冠動脈痙縮 |
|---|
| 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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Report
(4 results)
Research Products
(93 results)
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[Journal Article] Effects of a highly selective acetylcholine-activated K^+ channel blocker on experimental atrial fibrillation.2011
Author(s)
Machida T., Hashimoto N., Kuwahara I., Ogino Y., Matsuura J., Yamamoto W., Itano Y., Zamma A., Matsumoto R., Kamon J., Kobayashi T., Ishiwata N., Yamashita T., Ogura T., Nakaya H.
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Journal Title
Circ Arrhythm Electrophysiol. 4
Pages: 94-102
Related Report
Peer Reviewed
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[Journal Article] J-RHYTHM Investigators. Impact of drug alteration to maintain rhythm control in paroxysmal atrial fbrillation -Subanalysis from J-RHYTHM study-2010
Author(s)
Endo A., Kohsaka S., Suzuki S., Atarashi, H., Kamakura S., Sakurai M., 中谷晴昭, Fukatani M., Mitamura H., Yamazaki T., Yamashita T., Ogawa S.
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Journal Title
Circ J. 74
Pages: 870-875
Related Report
Peer Reviewed
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[Journal Article] Cardiac mast cells cause atrial fibrillation through PDGF-A-mediated fibrosis in pressure-overloaded mouse hearts.2010
Author(s)
Liao C.-h., Akazawa H., Tamagawa M., Ito K., Yasuda N., Kudo Y., Yamamoto R., Ozasa Y., Fujimoto M., Wang P., Nakauchi H., Nakaya H., Komuro I.
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Journal Title
J Clin Invest. 120
Pages: 242-253
Related Report
Peer Reviewed
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[Journal Article] PDK1 coordinates survival pathways and beta-adrenergic response in the heart.2009
Author(s)
Ito K, Akazawa H, Tamagawa M, Furukawa K, Ogawa W, Yasuda N, Kudo Y, Liao CH, Yamamoto R, Sato T, Molkentin JD, Kasuga M, Noda T, Nakaya H., Komuro I.
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Journal Title
Proc Natl Acad Sci USA. 106
Pages: 8689-8694
Related Report
Peer Reviewed
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