Roles of ion channels in regulation of acetylcholine-mediated vasoconstrictions in umbilical cords of rabbit/rats.
Roles of ion channels in regulation of acetylcholine-mediated vasoconstrictions in umbilical cords of rabbit/rats.
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DOI：
10.1016/j.reprotox.2016.07.003
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发表时间：
2016-10
期刊：
影响因子：
--
通讯作者：
Xu Z
中科院分区：
文献类型：
--
作者：
Zhu Z;Tang J;Zhou X;Xiang S;Zhu X;Li N;Shi R;Zhong Y;Zhang L;Sun M;Xu Z
我们最近证明乙酰胆碱（ACh）在脐带中产生可靠的血管收缩作用。本研究探讨了不同拮抗剂的可能机制。ACh介导的血管收缩被电压操纵性钙通道拮抗剂硝苯地平或肌醇-1，4，5-三磷酸介导的钙释放拮抗剂2-氨基乙基二苯硼酸盐抑制，表明细胞外和细胞内钙调节ACh刺激的脐收缩。细胞内Ca ~（2+）浓度增加的同时，血管收缩ACh在脐血管。抑制大电导钙依赖性钾（BK）通道增强ACh介导的收缩，而抑制电压依赖性钾（K+），内向整流性K+和ATP敏感性K+通道没有影响。孵育与特定的K+通道抑制剂表明，乙酰胆碱抑制BK电流，而不是4-氨基吡啶敏感的K+通道电流。结果提示，脐带血管对胆碱能信号的反应具有特殊性。乙酰胆碱刺激的脐血管收缩通过毒蕈碱受体亚型1/3-蛋白激酶C/环加氧酶-BK通道途径介导。
We recently demonstrated that acetylcholine (ACh) produced reliable vasoconstrictions in the umbilical cords. This study investigated the possible mechanisms with different antagonists. ACh-mediated vasoconstrictions were decreased by voltage-operated calcium (Ca2+) channels antagonist nifedipine or inositol-1,4,5-trisphosphate-mediated Ca2+ release antagonist 2-aminoethyl diphenylborinate, indicating that both extracellular and intracellular calcium modulated the ACh-stimulated umbilical contraction. Intracellular Ca2+ concentrations were increased simultaneously with vasoconstrictions by ACh in the umbilical vessels. Inhibiting large-conductance calcium-dependent potassium (BK) channels enhanced ACh-mediated contraction, whereas inhibiting voltage dependent potassium (K+), inward rectifier K+ and ATP-sensitive K+ channels had no effects. Incubation with specific K+ channel inhibitors showed that ACh suppressed BK currents rather than 4-aminopyridine-sensitive K+ channels currents. The results suggested that blood vessels in umbilical cords had special characteristics in response to cholinergic signals. ACh-stimulated umbilical vasoconstrictions were mediated via muscarinic receptor subtype 1/3–protein kinase C/cyclooxygenase-BK channel pathways.
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