ROLE OF ATP-SENSITIVE POTASSIUM CHANNELS IN THE BASILAR ARTERY

ROLE OF ATP-SENSITIVE POTASSIUM CHANNELS IN THE BASILAR ARTERY
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DOI:
10.1152/ajpheart.1993.264.1.h8
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发表时间:
1993-01-01
影响因子:
--
通讯作者:
HEISTAD, DD
HEISTAD, DD
中科院分区:
其他
文献类型:
--
作者:
FARACI, FM;HEISTAD, DD

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本研究验证了ATP敏感性钾通道激活产生血管舒张并有助于基底动脉对乙酰胆碱的扩张反应的假设。通过麻醉大鼠的颅窗测量基底动脉的直径(基线直径= 245 +/- 14 μ m,平均值+/- SE)。RP 52891(1 μ M)是ATP敏感性钾通道的直接激活剂,可使基底动脉直径增加33 +/-5%。格列本脲(1 μ M),ATP敏感性钾通道的抑制剂,没有改变基线直径,但消除了基底动脉对RP 52891的反应。局部应用乙酰胆碱(10 μ M)3分钟,在30秒时产生33 +/- 6%的峰值扩张,并产生17 +/-4%的直径持续增加。格列本脲不抑制基底动脉对乙酰胆碱的扩张反应。硝基-L-精氨酸甲酯(10和100 μ M),抑制内皮衍生的舒张因子(EDRF)的合成,产生浓度依赖性抑制基底动脉扩张的乙酰胆碱反应。因此,ATP敏感性钾通道是功能性的,但似乎不影响基底动脉的基础张力。基底动脉对乙酰胆碱的扩张反应依赖于EDRF的形成,但不依赖于格列本脲敏感性钾通道的活性。
This study examined the hypothesis that activation of ATP-sensitive potassium channels produces vasodilatation and contributes to dilator responses of the basilar artery to acetylcholine in vivo. Diameter of the basilar artery (baseline diam = 245 +/- 14 mum, means +/- SE) was measured through a cranial window in anesthetized rats. RP52891 (1 muM), a direct activator of ATP-sensitive potassium channels, increased the diameter of the basilar artery by 33 +/- 5%. Glibenclamide (1 muM), an inhibitor of ATP-sensitive potassium channels, did not alter baseline diameter but abolished responses of the basilar artery to RP52891. Topical application of acetylcholine (10 muM) for 3 min produced peak dilatation of 33 +/- 6% at 30 s and produced a sustained increase in diameter of 17 +/- 4%. Glibenclamide did not inhibit dilator responses of the basilar artery to acetylcholine. Nitro-L-arginine methyl ester (10 and 100 muM), which inhibits synthesis of endothelium-derived relaxing factor (EDRF), produced concentration-dependent inhibition of dilatation of the basilar artery in response to acetylcholine. Thus ATP-sensitive potassium channels are functional but do not appear to influence basal tone of the basilar artery. Dilator responses of the basilar artery to acetylcholine are dependent on formation of EDRF but not dependent on activity of glibenclamide-sensitive potassium channels.