Bradykinin Mediation of Ca2+-Activated K+ Channels Regulates Coronary Blood Flow in Ischemic Myocardium
Bradykinin Mediation of Ca2+-Activated K+ Channels Regulates Coronary Blood Flow in Ischemic Myocardium
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Ca2 激活 K 通道的缓激肽介导调节缺血心肌中的冠状动脉血流
DOI：
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发表时间：
1997
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影响因子：
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通讯作者：
MasatsuguHori
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文献类型：
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作者：
KoichiNode;MasafumiKitakaze;HiroakiKosaka;TetsuoMinamino;MasatsuguHori
内皮依赖性超极化因子通过打开Ca2+激活的K+ (KCa)通道来放松血管平滑肌。探讨心肌缺血时KCa通道开放在冠状动脉血管扩张中的作用。方法与结果采用颈动脉体外旁路管灌注左冠状动脉前降支。冠状动脉内给药缓激肽增加了硝酸合酶抑制剂ng -硝基精氨酸甲酯（L-NAME）治疗犬的冠状动脉血流量（CBF）；这种作用被KCa通道阻滞剂iberiotoxin完全抑制。在接受L-NAME治疗的狗中，阻断旁路管使CBF降至基线值的三分之一，之后冠状动脉灌注压保持不变。在冠状动脉内给予iberiotoxin 20分钟进一步降低CBF（从33±2到19±2 mL·100 g−1·min−1，P< 0.01），部分起酥油和乳酸提取物。
Background Endothelium-dependent hyperpolarizing factor relaxes vascular smooth muscles by opening the Ca2+-activated K+ (KCa) channels. The role of the opening of KCa channels in coronary vasodilation during myocardial ischemia was investigated. Methods and Results The left anterior descending coronary arteries of open-chest dogs were perfused with blood through an extracorporeal bypass tube from the carotid artery. Intracoronary administration of bradykinin increased coronary blood flow (CBF) in dogs treated with NG-nitro-l-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase; this effect was completely inhibited by the KCa channel blocker iberiotoxin. In dogs treated with L-NAME, the bypass tube was occluded to reduce CBF to one third of the baseline value, after which coronary perfusion pressure was maintained constant. Intracoronary administration of iberiotoxin for 20 minutes further decreased CBF (from 33±2 to 19±2 mL·100 g−1·min−1, P<.01), fractional shortening, and lactate extrac...