Functional role of ATP-sensitive K^+ channel in vascular endothelial cells

血管内皮细胞中ATP敏感性K^通道的功能作用

• 批准号: 20590249
• 负责人: NAKAYA Haruaki
• 金额: $ 3.08万
• 依托单位: Chiba University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20590249/
• 关键词: 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

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.

据报道，在Kir6.2缺乏或SUR2缺乏的小鼠中观察到prinzmetal型心绞痛。为了确定内皮细胞中ATP敏感的K^+（KATP）通道的功能障碍参与KIR6.2缺陷或SUR2缺陷的小鼠的血管痉挛性心绞痛的开发，我们通过使用PatchAmpAlp Termique和Gene prs ccr来评估对K^+通道开启的电子生理响应。 K^+通道开瓶器未能影响从野生型小鼠和培养的小鼠内皮细胞（UV细胞）的血管内皮细胞中的膜电位。在这些内皮细胞中，几乎未检测到与KATP通道有关的离子通道基因。相比之下，RT-PCR可以检测到KiR6.1和SUR2B的小鼠尿膀胱mRNA。 K^+通道揭示杆pinacidil在野生型和Kir6.2缺乏小鼠的内脏平滑肌细胞中诱导KATP电流，而不是Kir6.1缺陷小鼠的小鼠。这些结果表明，血管内皮细胞中的KATP通道不太可能在诱导小鼠的血管痉挛性绞痛中起重要作用。

项目成果

Ghrelin reduces infarct size via activation of PI3-k and mitochondrial ATP-sensitive K^+ channels in rabbits hearts

Ghrelin 通过激活兔心脏中的 PI3-k 和线粒体 ATP 敏感 K^ 通道来减少梗塞面积

• 发表时间: 2010
• 作者: Rafiq K;Nakano D;Hitomi H;Daisuke Yamamoto;稲村直樹
• 通讯作者: 稲村直樹

Dose Anti-Inflammatory Action of Amiodarone Explain the High Efficancy in Patients With Heart Failure?

胺碘酮的剂量抗炎作用解释了心力衰竭患者的高疗效？

• 发表时间: 2009
• 期刊: Cir J. 73
• 作者: 中山均;趙晶;吉栖正典;Nakaya H
• 通讯作者: Nakaya H

Mechanism of pharmacological postconditioning by ghrelin after ischemia/reperfusion in rabbit hearts.

兔心脏缺血/再灌注后生长素释放肽的药理后处理机制。

• 发表时间: 2009
• 作者: 原田新太郎;稲村直樹;西田洋文;松本明郎;中谷晴昭
• 通讯作者: 中谷晴昭

グレリンのミトコンドリアATP感受性カリウムチャネルとホスファチジルイノシトール3キナーゼを介する心筋保護作用

线粒体 ATP 敏感钾通道和磷脂酰肌醇 3 激酶介导的生长素释放肽的心脏保护作用

• 发表时间: 2009
• 作者: 稲村直樹;西田洋文;原田新太郎;友野尚弘;花開孝宏;松本明郎;中谷晴昭
• 通讯作者: 中谷晴昭

Effects of antiarrhythmic drugs on the hyperpolarization-activated cyclic nucleotide-gated channel current.

• DOI: 10.1254/jphs.08312fp
• 发表时间: 2009
• 期刊: Journal of pharmacological sciences
• 影响因子: 3.5
• 作者: Atsushi Tamura;T. Ogura;H. Uemura;Y. Reien;T. Kishimoto;T. Nagai;I. Komuro;M. Miyazaki;H. Nakaya