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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

基本信息

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

项目摘要

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缺陷型或SUR 2缺陷型小鼠中观察到Prinzmetal型心绞痛。为了确定内皮细胞ATP敏感性K^+（KATP）通道功能障碍是否与Kir6.2缺陷或SUR 2缺陷小鼠血管痉挛性心绞痛的发生有关，我们采用膜片钳技术和真实的时间PCR技术评估了内皮细胞对K^+通道开放剂的电生理反应和基因表达。K^+通道开放剂不能影响从野生型小鼠肺组织分离的血管内皮细胞和培养的小鼠内皮细胞（UV细胞）的膜电位。在这些内皮细胞中几乎没有检测到与KATP通道相关的离子通道基因。而在小鼠膀胱组织中，可通过RT-PCR检测到Kir6.1和SUR 2B的mRNA。K^+通道开放剂吡那地尔在野生型和Kir6.2缺陷小鼠的内脏平滑肌细胞中诱导KATP电流，但在Kir6.1缺陷小鼠的内脏平滑肌细胞中不诱导。提示血管内皮细胞KATP通道在血管痉挛性心绞痛的发生中可能不起重要作用。

项目成果

期刊论文数量（0）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

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
通讯作者：
Atsushi Tamura;T. Ogura;H. Uemura;Y. Reien;T. Kishimoto;T. Nagai;I. Komuro;M. Miyazaki;H. Nakaya

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