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缝隙连接/嘌呤能信号在雄性金黄地鼠骨骼肌收缩时毛细血管间通讯中的作用。

The role of pannexin/purinergic signaling in intervascular communication from capillaries during skeletal muscle contraction in male Golden hamsters.

机构信息

Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.

出版信息

Physiol Rep. 2024 Jun;12(12):e16113. doi: 10.14814/phy2.16113.

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 M), purinergic receptor antagonist suramin (SUR 10 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

我们试图确定缝隙连接/嘌呤能依赖性信号在介导由骨骼肌收缩引起的毛细血管刺激引起的传导性血管舒张中的生理相关性。使用仓鼠提睾肌和活体显微镜,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。在没有和存在缝隙连接阻滞剂甲氟喹(MEF;10 μM)、嘌呤能受体拮抗剂苏拉明(SUR 10 μM)和缝隙连接解偶联剂氟烷(HALO,0.07%)的情况下,毛细血管以低收缩(6 和 60CPM)和刺激频率(4 和 40 Hz)进行刺激肌肉收缩和上游小动脉观察部位之间的位置。在 6CPM 时引发的传导性血管舒张被 HALO 抑制,而在 60CPM 时引发的血管舒张被 MEF 和 SUR 抑制。在 4 Hz 时引发的传导反应被 MEF 抑制,而在 40 Hz 时的血管舒张不受任何阻滞剂的影响。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缝隙连接/嘌呤能依赖性途径,该途径似乎依赖于刺激参数。我们的数据强调了缝隙连接/嘌呤能途径在促进毛细血管和上游小动脉微血管之间的通讯中的生理重要性,因此表明该途径可能在响应骨骼肌收缩调节血流方面发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec52/11186745/4b614a2696a1/PHY2-12-e16113-g015.jpg

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