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首页> 外文期刊>Medicine and science in sports and exercise >Hyperosmolarity causes BK Ca-dependent vasodilatations in rat skeletal muscle arteries.
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Hyperosmolarity causes BK Ca-dependent vasodilatations in rat skeletal muscle arteries.

机译：高渗性会在大鼠骨骼肌动脉中引起BK Ca依赖性血管舒张。

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PURPOSE: The release of different metabolites during skeletal muscle contraction causes a pronounced increase in extracellular osmolarity (hyperosmolarity (HO)). HO has been considered as a possible mediator of the exercise hyperemia. In the present study, we investigated the vasodilatory effect of physiologically relevant increases in the extracellular osmolarity in isolated rat gluteal muscle arterioles. In addition, we analyzed the underlying mechanisms of the HO-induced vasodilatations. METHODS: Rat gluteal arteries were isolated and mounted in an organ bath for isometric tension recording. After precontraction with norepinephrine, 20, 40, or 60 mmol x L(-1) sucrose, mannitol, or urea was added in control conditions, after removal of the endothelium or in the presence of inhibitors. RESULTS: Application of sucrose or mannitol induced large and fast concentration-dependent vasodilatations (up to 46.15% with 60 mmol x L(-1) sucrose). Removal of the vascular endothelium had no effect on this relaxation. Inhibition of the Na+/K+ pumps with ouabain, the Kir IR channels with Ba2+ and the K ATP channels with glibenclamide did not alter the HO-induced relaxations. Incubation with the KCa channel blockers charybdotoxin and apamin significantly inhibited sucrose-induced vasodilatations. In addition, application of the specific BK Ca channel blocker iberiotoxin significantly decreased the HO-induced vasodilatations. CONCLUSION: The present study shows that an increase in the extracellular osmolarity elicits strong, fast, and long-lasting relaxations of rat skeletal muscle arterioles, suggesting an important role both at the onset and during the steady-state phase of an exercise bout. Vascular smooth muscle BK Ca channels seem to play a crucial role in the HO-induced vasorelaxations.
机译：目的：骨骼肌收缩过程中不同代谢物的释放导致细胞外渗透压（高渗压（HO））的明显增加。 HO被认为是运动性充血的一种可能的介质。在本研究中，我们调查了离体大鼠臀肌小动脉中细胞外渗透压的生理相关增加的血管舒张作用。此外，我们分析了HO诱导的血管舒张的潜在机制。方法：分离大鼠臀动脉并将其安装在器官浴中以记录等距张力。用去甲肾上腺素预收缩后，在对照条件下，除去内皮后或存在抑制剂的情况下，在对照条件下加入20、40或60 mmol x L（-1）蔗糖，甘露醇或尿素。结果：蔗糖或甘露醇的应用引起大而快速的浓度依赖性血管舒张作用（使用60 mmol x L（-1）蔗糖可达到46.15％）。血管内皮的去除对此松弛没有影响。哇巴因对Na + / K +泵的抑制，Ba2 +对Kir IR通道的抑制和格列本脲对K ATP通道的抑制不会改变HO诱导的弛豫。与KCa通道阻滞剂Charybdotoxin和Apamin一起孵育可显着抑制蔗糖诱导的血管舒张。此外，特定BK Ca通道阻滞剂埃博毒素的应用显着减少了HO诱导的血管舒张。结论：本研究表明，细胞外渗透压的增加引起大鼠骨骼肌小动脉强烈，快速和持久的松弛，表明在运动发作的开始阶段和稳态阶段均起重要作用。血管平滑肌BK Ca通道似乎在HO诱导的血管舒张中起关键作用。

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