期刊
EXPERIMENTAL BIOLOGY AND MEDICINE
卷 228, 期 5, 页码 474-480出版社
SOC EXPERIMENTAL BIOLOGY MEDICINE
DOI: 10.1177/15353702-0322805-09
关键词
carbon monoxide; chemical modification; gasotransmitter; K-Ca channels; nitric oxide
The activation of big-conductance K-Ca channels in vascular smooth muscle cells by carbon monoxide (CO) has been demonstrated previously. One specific target of CO on K-Ca channel proteins is the histidine residue. The roles of other amino acid residues on the functionality of K-Ca. channels, as well as their reactions to CO, have been unclear. In the present study, the cell-free single channel recording technique was used to investigate the chemical modification of K-Ca channels by CO and other chemical agents. The modification of negatively charged carboxyl groups and the E-amino group of lysine did not affect the open probability, but decreased single-channel conductance of K-Ca channels. When sulfhydryl groups of cysteine were modified with N-ethylmaleimide, the open probability of K-Ca channels was decreased, but single-channel conductance was not affected. None of the above chemical modifications affected the CO-induced increase in the open probability of K-Ca channels. However, N-ethylmaleimide treatment reduced the stimulatory effect of nitric oxide (NO) on K-Ca channels. Finally, pretreatment of smooth muscle cells with NO abolished the effects of subsequently applied CO on K-Ca channel proteins. Our study demonstrates that CO and NO acted on different amino acid residues of K-Ca channel proteins. The interaction of CO and NO determines the functional status of K-Ca channels in vascular smooth muscle cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据