Progression of cardiac potassium current modification after brief exposure to reactive oxygen.
Progression of cardiac potassium current modification after brief exposure to reactive oxygen.
复制标题
短暂暴露于活性氧后心脏钾电流改变的进展。
DOI：
10.1016/0022-2828(95)90046-2
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发表时间：
1995
影响因子：
5
通讯作者：
Valenzeno,D
中科院分区：
文献类型：
--
作者：
Tarr,M;Arriaga,E;Valenzeno,D
我们以前报道过，通过照亮光敏剂玫瑰红（RB）产生的单线态氧（1O2）抑制单个蛙心房细胞的延迟整流钾电流（IK）。考虑到1o2的短暂寿命，人们可能会期望在短暂暴露于rb生成的1o2后，IKmodification很快达到稳定状态。在这里，我们报告说，与预期相反，ikk可能需要几十秒才能达到一个新的稳态。我们将使用术语“进展”来指在照明停止后发生的当前修改的组成部分。为了深入了解这一过程的机制，我们研究了(1)RB照明期间和之后的膜电位，以及(2)照明期间的IKactivation水平对其时间进程和幅度的影响。我们发现有利于钾通道开放状态的条件也有利于进展，增加了其时间进程和幅度。当我被激活时，照明会产生非常缓慢的进程（几十秒）。相比之下，当ik未被激活时，照明没有产生进展；在2 s照明周期内完成改造。这些发现表明，进展是由钾通道状态转变的动力学引起的，而不是由最初暴露于o2时产生的长寿命反应中间体引起的。
We reported previously that singlet oxygen (1O2), generated by illuminating the photosensitizer rose bengal (RB), suppressed the delayed rectifier potassium current (IK) in single frog atrial cells. Considering the brief lifetime of1O2, one might expect IKmodification to reach a steady-state soon after a brief exposure to RB-generated1O2. Here we report that, contrary to expectations, tens of seconds can be required for IKto reach a new steady-state. We will use the term “progression” to refer to the component of current modification which occurs after cessation of illumination. To gain insight into the mechanism of progression, we investigated how its time course and magnitude were affected by (1) membrane potential during and following RB illumination, and (2) the level of IKactivation during illumination. We found that conditions which favored the open state of the potassium channel also favored progression, increasing both its time course and magnitude. Illumination while IKwas activated produced significant progression having a very slow time course (tens of seconds). By comparison, illumination when IKwas not activated produced no progression; IKmodification was completed during the 2 s illumination period. These findings suggest progression results from the kinetics of potassium channel state transitions rather than from a long-lived reactive intermediate produced during the initial1O2exposure.