Nitric oxide directly activates calcium‐activated potassium channels from rat brain reconstituted into planar lipid bilayer

FEBS Letters

Shin, Jung Hoon²  Uhm, Dae-Yong¹  Suh, Chang Kook²  Park, Eun Joo²  Chung, Sungkwon³ 

[1] Department of Physiology, Sung Kyun Kwan University College of Medicine, Suwon 440-746, South Korea;Department of Physiology and Biophysics, Inha University College of Medicine, Inchon 402-751, South Korea;Department of Physiology, Chung-Ang University College of Medicine, Seoul 156-756, South Korea

关键词: Calcium-activated potassium channel;    Nitric oxide;    Lipid bilayer;    Streptozotocin;   

DOI  :  10.1016/S0014-5793(97)01144-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Using the planar lipid bilayer technique, we tested whether NO directly activates calcium-activated potassium (Maxi-K) channels isolated from rat brain. We used streptozotocin (STZ) as NO donor, and the NO release was controlled with light. In the presence of 100–800 μM STZ, the Maxi-K channel activity increased up to 3-fold within several tens of seconds after the light was on, and reversed to the control level several minutes after shutting off the light. Similar activation was observed with other NO donors such as S-nitroso-N-acetylpenicillamine and sodium nitroprusside. The degree of activity increase was dependent upon the initial open probability (P _init). When the P _init was lower, the activity increase was greater. These results demonstrate that NO can directly affect the Maxi-K channel activity, and suggest that the Maxi-K channel might be one of the physiological targets of NO in brain.

【 授权许可】

Unknown