PDF(Pubmed)
Abstract：
We sought to determine the physiological relevance of pannexin/purinergic-dependent signaling in mediating conducted vasodilation elicited by capillary stimulation through skeletal muscle contraction. Using hamster cremaster muscle and intravital microscopy we stimulated capillaries through local muscle contraction while observing the associated upstream arteriole. Capillaries were stimulated with muscle contraction at low and high contraction (6 and 60CPM) and stimulus frequencies (4 and 40 Hz) in the absence and presence of pannexin blocker mefloquine (MEF; 10-5 M), purinergic receptor antagonist suramin (SUR 10-5 M) and gap-junction uncoupler halothane (HALO, 0.07%) applied between the capillary stimulation site and the upstream arteriolar observation site. Conducted vasodilations elicited at 6CPM were inhibited by HALO while vasodilations at 60CPM were inhibited by MEF and SUR. The conducted response elicited at 4 Hz was inhibited by MEF while the vasodilation at 40 Hz was unaffected by any blocker. Therefore, upstream vasodilations resulting from capillary stimulation via muscle contraction are dependent upon a pannexin/purinergic-dependent pathway that appears to be stimulation parameter-dependent. Our data highlight a physiological importance of the pannexin/purinergic pathway in facilitating communication between capillaries and upstream arteriolar microvasculature and, consequently, indicating that this pathway may play a crucial role in regulating blood flow in response to skeletal muscle contraction.
摘要：
我们试图确定pannexin/嘌呤能依赖性信号在介导通过骨骼肌收缩的毛细血管刺激引起的传导血管舒张中的生理相关性。使用仓鼠提子肌肉和活体显微镜，我们通过局部肌肉收缩刺激毛细血管，同时观察相关的上游小动脉。在不存在和存在pannexin阻滞剂甲氟喹（MEF;10-5M）的情况下，在低收缩和高收缩（6和60CPM）和刺激频率（4和40Hz）下刺激毛细血管，嘌呤能受体拮抗剂苏拉明（SUR10-5M）和间隙连接解偶联剂氟烷（HALO，0.07％）施加在毛细血管刺激部位和上游小动脉观察部位之间。在6CPM引起的传导血管舒张被HALO抑制,而在60CPM引起的血管舒张被MEF和SUR抑制。在4Hz下引起的传导反应被MEF抑制,而在40Hz下的血管舒张不受任何阻断剂的影响。因此,通过肌肉收缩刺激毛细血管引起的上游血管舒张依赖于pannexin/嘌呤能依赖性通路,该通路似乎依赖于刺激参数.我们的数据强调了pannexin/嘌呤能途径在促进毛细血管和上游小动脉微脉管系统之间的联系方面的生理重要性，因此,这表明该途径可能在调节骨骼肌收缩时的血流中起关键作用。
