Zhao Li-min, Xu Yong-jian, Zhang Zhen-xiang, Cheng Dong-jun, Ni Wang
Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2006 Aug;22(3):348-51.
To investigate the role of delayed rectifier K+ channel (Kv), Ca2+ -activated K+ channel (K(Ca)) and ATP-sensitive K+ channel (K(ATP)) in the regulation of the resting and contracting tone of human control and passively sensitized bronchial smooth muscle (BSM).
The regulating effects of the three K+ channels on the tone of human BSM (HBSM) were observed by measuring the isometric tone of bronchial rings in vitro.
(1) The contraction of passively sensitized bronchial ring was significantly increased by histamine. (2) Kv blocker 4-aminopyridine (4-AP) caused concentration dependent contraction in resting bronchial rings of two groups, and the contraction sensitivity of the sensitized group rings was significantly stronger than that of control, that is, the negative logarithm of the drug concentration causing 50% of maximal effect (pD2) of the sensitized group rings were significantly larger than that of control rings, but there was no difference in the maximal effect (Emax) of two groups; Kca blocker tetraethylammonium (TEA) and K(ATP) blocker glibenclamide (Glib) had no such effects as those of 4-AP. (3) After pretreatment with 4-AP, the contraction of the control rings could significantly increased by histamine. After 4-AP treatment the Emax was significantly larger than that before 4-AP treatment. But the sensitized group rings had no such change, there was no significant difference in Emax before and after 4-AP treatment.
(1) Not K(Ca) and K(ATP) but Kv participated in regulation of the resting tone of HBSM. (2) The activity of Kv decreased in bronchial smooth muscle passively sensitized by asthmatic serum compared with that of nonsensitized group. This change might be involved in the mechanism of asthma.
研究延迟整流钾通道（Kv）、钙激活钾通道（K（Ca））和ATP敏感性钾通道（K（ATP））在调节人对照及被动致敏支气管平滑肌（BSM）静息和收缩张力中的作用。
通过体外测量支气管环的等长张力，观察三种钾通道对人BSM（HBSM）张力的调节作用。
（1）组胺显著增加被动致敏支气管环的收缩。（2）Kv阻滞剂4-氨基吡啶（4-AP）在两组静息支气管环中引起浓度依赖性收缩，致敏组环的收缩敏感性明显强于对照组，即引起致敏组环最大效应50%的药物浓度的负对数（pD2）明显大于对照环，但两组的最大效应（Emax）无差异；Kca阻滞剂四乙铵（TEA）和K（ATP）阻滞剂格列本脲（Glib）没有4-AP那样的作用。（3）用4-AP预处理后，组胺可使对照环的收缩显著增加。4-AP处理后Emax明显大于4-AP处理前。但致敏组环无此变化，4-AP处理前后Emax无显著差异。
（1）参与调节HBSM静息张力的是Kv而非K（Ca）和K（ATP）。（2）与未致敏组相比，哮喘血清被动致敏的支气管平滑肌中Kv活性降低。这种变化可能参与了哮喘的发病机制。
