Nakamoto Tomoko, Matsukawa Kanji
Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8551, Japan.
J Appl Physiol (1985). 2007 Jun;102(6):2112-20. doi: 10.1152/japplphysiol.01344.2006. Epub 2007 Feb 22.
Feedback regulation by activation of mechanosensitive afferents in the exercising muscle causes the cardiovascular and sympathetic nerve responses, which follow tension development and are almost identical between static contraction and passive stretch. The precise location of the mechanoreceptors contributing to the exercise pressor reflex, however, remained unknown. To test the hypothesis that the mechanoreceptors will be located around the myotendinous junction to monitor a change in muscle tension than a change in muscle length, we examined the reflex cardiovascular responses to passive stretch of the triceps surae muscle in anesthetized rats with three interventions; systemic injection of gadolinium, cutting the Achilles tendon, and local injection of lidocaine into the myotendinous junction. Gadolinium (42 micromol/kg iv) blunted the increases in heart rate and mean arterial blood pressure during passive stretch by 36 and 22-26%, respectively, suggesting that the reflex cardiovascular responses were evoked by stimulation of muscle mechanosensitive receptors. The cardiovascular responses to passive stretch were not different between the cut Achilles tendon and the intact tendon in the same rats, suggesting that any mechanoreceptors, terminated in the more distal part of the tendon, did not contribute to the reflex cardiovascular responses. Lidocaine (volume, 0.04-0.1 ml) injected into the myotendinous junction blunted the stretch-induced increases in heart rate and mean arterial blood pressure by 37-49 and 27-34%, respectively. We conclude that the muscle mechanosensitive receptors evoking the reflex cardiovascular responses at least partly locate at or close to the myotendinous junction of the Achilles tendon.
运动肌肉中机械敏感传入神经的激活所引起的反馈调节会导致心血管和交感神经反应，这些反应跟随张力发展，并且在静态收缩和被动拉伸之间几乎相同。然而，参与运动升压反射的机械感受器的确切位置仍然未知。为了验证机械感受器将位于肌腱结合处周围以监测肌肉张力变化而非肌肉长度变化的假设，我们通过三种干预措施研究了麻醉大鼠中腓肠肌被动拉伸时的反射性心血管反应；全身注射钆、切断跟腱以及向肌腱结合处局部注射利多卡因。钆（42微摩尔/千克静脉注射）使被动拉伸期间心率和平均动脉血压的升高分别降低了36%和22%-26%，这表明反射性心血管反应是由肌肉机械感受器的刺激所诱发的。在同一只大鼠中，切断跟腱和完整跟腱时被动拉伸的心血管反应没有差异，这表明终止于肌腱更远端的任何机械感受器对反射性心血管反应没有贡献。向肌腱结合处注射利多卡因（体积，0.04-0.1毫升）使拉伸诱导的心率和平均动脉血压升高分别降低了37%-49%和27%-34%。我们得出结论，诱发反射性心血管反应的肌肉机械感受器至少部分位于跟腱的肌腱结合处或其附近。
