摘要
目的探讨α1肾上腺素受体在调控快激活延迟整流钾电流(Ikr)中的作用。方法制备豚鼠心肌细胞,采用全细胞膜片钳技术记录心肌细胞Ikr。心肌细胞采用α1肾上腺素受体激动剂苯肾上腺素0.1μmol/L处理后分为五组:A组作为对照;B1、B2、B3和B4组分别以α1肾上腺素受体阻滞剂哌唑嗪1μmol/L、α1肾上腺素受体α1A亚型阻滞剂5-甲基乌拉地尔1μmol/L、α1肾上腺素受体α1B亚型阻滞剂氯乙基可乐定10μmol/L和α1肾上腺素受体α1D亚型阻滞剂BMY-7378 1nmol/L干预,比较干预前后心肌细胞Ikr的变化。结果 B1组和B2组心肌细胞Ikr降为干预前的0.92±0.07和0.97±0.04,高于A组的0.67±0.03(P<0.01),而B3和B4组心肌细胞Ikr降为干预前的0.64±0.06和0.73±0.07,与A组相仿(P>0.05)。结论α1肾上腺素受体激活可降低心肌细胞Ikr;该作用主要通过α1肾上腺素受体和α1A亚型介导。
Objective To explore the effects of α1-adrenergic receptor on regulation of the rapid activation of delayed rectifier potassium current（Ikr）. Methods Guinea pig ventricular myocytes were prepared. Ikr was recorded by whole-cell patch-clamp technique. Myocardial cells were treated with 0. 1μmol/L α1 epinephrine agonist phenylephrine, which were assigned into 5 groups of A（control）, B1 （intervened withal adrenaline receptor blocker prazosin 1μmol/L, 132 （intervened withα1A adrenaline receptor blocker 5-methylurapidil 1 μmol/L）, 133 （intervened with alB adrenaline receptor blocker cholorethylclonidine 10 μmol/L） and B4（intervened with α1D adrenaline receptor blocker BMY-7378 1 nmol/L）. The value of Ikr was compared before and after intervention. Results After treatment, the values of Iuwere decreased to 0.92±0. 07 and 0. 97!0. 04 of before in groups of B1 and 132,which were higher than 0. 67±0. 03 in group A（P〈0. 01）. The decreases of Iuafter intervention in groups of 133 and B4（0. 64±0. 06 and 0. 73±0. 07） were not significantly different from those in group A （P〈0. 05）. Conclusion The activation of α1-adrenergic receptor can reduce Ikr of myocardial cells, which is mainly mediated via alA-adrenergic receptor.
出处
《江苏医药》
CAS
北大核心
2014年第3期255-258,共4页
Jiangsu Medical Journal
基金
国家自然科学基金青年基金(81100123)
关键词
Α1肾上腺素受体
钾电流
α1-Adrenergic receptoriPotassium current
