Large-conductance Ca2+-activated K+ currents blocked and impaired by homocysteine in human,and rat mesenteric artery smooth muscle cells

被引:27
作者
Cai, Benzhi
Gong, Dongmei
Pan, Zhenwei
Liu, Yu
Qian, Hong
Zhang, Yong
Jiao, Jundong
Lu, Yanjie
Yang, Baofeng
机构
[1] Harbin Med Univ, Dept Pharmacol, Harbin 150081, Peoples R China
[2] Province State Key Lab, Harbin 150086, Peoples R China
基金
中国国家自然科学基金;
关键词
BKCa; homocysteine; mesenteric artery smooth muscle cells; electrophysiology;
D O I
10.1016/j.lfs.2007.03.003
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Plenty of evidence suggests that increased blood levels of homocysteine (Hey) are an independent risk factor for the development of vascular diseases, but the underlying mechanisms are not well understood. It is well known that the larger conductance Ca2+-activated K+ channels (BKCa) play an essential role in vascular function, so the present study was conducted to determine direct effects of Hey on BKCa, channel properties of smooth muscle cells. Whole-cell patch-clamp recordings were made in mesenteric artery smooth muscle cells isolated from normal rat and patients to investigate effects of 5, 50 and 500 mu M Hey on BKCa, the main current mediating vascular responses in these cells. In human artery smooth muscle cells, maximum BKCa density (measured at + 60 mV) was inhibited by about 24% (n = 6, P < 0.05). In rat artery smooth muscle cells, maximum BKCa density was decreased by approximately 27% in the presence of 50 mu M Hey (n = 8, P < 0.05). In addition, when rat artery smooth muscle cells was treated with 50 VM Hey for 24 h, maximum BKCa density decreased by 58% (n = 5, P < 0.05). These data suggest that Hey significantly inhibited BKCa currents in isolated human and rat artery smooth muscle cells. BKCa reduced and impaired by elevated Hey levels might contribute to abnormal vascular diseases. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:2060 / 2066
页数:7
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