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ALTERATION OF ION CHANNELS IN VASCULAR SMOOTH MUSCLE IN HYPERTENSION

高血压时血管平滑肌离子通道的改变

基本信息

批准号：
11670686
负责人：
OHYA Yusuke
金额：
$ 1.34万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11670686/
关键词：
hypertension ion channel artery 平滑筋

项目摘要

Our progress during two years (1998-1999) are summarized as follows :1) Enhanced activation of voltage-operated calcium (Ca) channels in vascular smooth muscle cells from Dahl salt sensitive ratsDietary salt loading elevates blood pressure in Dahl salt sensitive rats. Arterial smooth muscle cells exhibited depolarized resting membrane potential and spontaneous electrical activity in rats after salt loading. We demonstrated by using the patch clamp method that activation of L-type calcium was enhanced in salt-loaded rats. Enhanced activation was especially evident near the resting potential, suggesting that this mechanism would contribute enhanced electrical activity of arterial tissues.2) Sodium-potassium (Na-K) pump in vascular smooth muscle cellsNa-K pump regulates intracellular ion concentration and membrane potential. We for the first time characterized Na-K pump of vascular smooth muscle cells by using the patch clamp method. Activation of Na-K pump depended on intracellular Na, extracellular K, temperature, and membrane potential. Sensitivity to ouabain of smooth muscle Na-K pump was high. Inhibition of Na-K pump by ouabain depolarized membrane potential, suggesting that Na-K pump would contribute to regulation of membrane potential in vascular smooth muscle cells.3) Potassium (K) channels in rat mesenteric arterial smooth muscleWe performed molecular identification of voltage-dependent K channels in smooth muscle of rat mesenteric arteries by immunohistochmistry. At least three components such as Kv1.2, Kv1.5, and Kv2.1 were identified. In patch clamp experiments, voltage dependent K currents were decreased in spontaneously hypertensive rats compared to normotensive control rats, Wistar Kyoto rats.

本实验室在1998-1999年两年的研究中取得了以下进展：1）Dahl盐敏感大鼠血管平滑肌细胞电压操纵性钙通道激活增强饮食盐负荷可使Dahl盐敏感大鼠血压升高。大鼠动脉平滑肌细胞在盐负荷后出现去极化静息膜电位和自发电活动。我们用膜片钳方法证明，盐负荷大鼠L型钙激活增强。在静息电位附近激活增强尤为明显，提示该机制可能有助于动脉组织电活动的增强。2）血管平滑肌细胞钠钾泵（Na-K）Na-K泵调节细胞内离子浓度和膜电位。我们首次用膜片钳技术对血管平滑肌细胞钠钾泵进行了表征。钠钾泵的激活取决于细胞内钠、细胞外钾、温度和膜电位。平滑肌钠钾泵对哇巴因敏感性高。哇巴因对钠钾泵的抑制使膜电位去极化，提示钠钾泵可能参与了血管平滑肌细胞膜电位的调节。3）大鼠肠系膜动脉平滑肌钾通道的研究至少有三个组件，如Kv1.2，Kv1.5和Kv2.1被确定。在膜片钳实验中，电压依赖性钾电流降低自发性高血压大鼠相比，血压正常的对照组大鼠，Wistar京都大鼠。