The Copenhagen Muscle Research Centre, Rigshospitalet, Denmark, Denmark.
J Appl Physiol (1985). 2009 Dec;107(6):1757-62. doi: 10.1152/japplphysiol.00638.2009. Epub 2009 Oct 1.
ATP has been proposed to play multiple roles in local skeletal muscle blood flow regulation by inducing vasodilation and modulating sympathetic vasoconstrictor activity, but the mechanisms remain unclear. Here we evaluated the effects of arterial ATP infusion and exercise on leg muscle interstitial ATP and norepinephrine (NE) concentrations to gain insight into the interstitial and intravascular mechanisms by which ATP causes muscle vasodilation and sympatholysis. Leg hemodynamics and muscle interstitial nucleotide and NE concentrations were measured during 1) femoral arterial ATP infusion (0.42 +/- 0.04 and 2.26 +/- 0.52 micromol/min; mean +/- SE) and 2) one-leg knee-extensor exercise (18 +/- 0 and 37 +/- 2 W) in 10 healthy men. Arterial ATP infusion and exercise increased leg blood flow (LBF) in the experimental leg from approximately 0.3 l/min at baseline to 4.2 +/- 0.3 and 4.6 +/- 0.5 l/min, respectively, whereas it was reduced or unchanged in the control leg. During arterial ATP infusion, muscle interstitial ATP, ADP, AMP, and adenosine concentrations remained unchanged in both legs, but muscle interstitial NE increased from approximately 5.9 nmol/l at baseline to 8.3 +/- 1.2 and 8.7 +/- 0.7 nmol/l in the experimental and control leg, respectively (P < 0.05), in parallel to a reduction in arterial pressure (P < 0.05). During exercise, however, interstitial ATP, ADP, AMP, and adenosine concentrations increased in the contracting muscle (P < 0.05), but not in inactive muscle, whereas interstitial NE concentrations increased similarly in both active and inactive muscles. These results suggest that the vasodilatory and sympatholytic effects of intraluminal ATP are mainly mediated via endothelial purinergic receptors. Intraluminal ATP and muscle contractions appear to modulate sympathetic nerve activity by inhibiting the effect of NE rather than blunting its local concentration.
三磷酸腺苷（ATP）被认为通过诱导血管舒张和调节交感神经血管收缩活性在局部骨骼肌血流调节中发挥多种作用，但机制尚不清楚。在这里，我们评估了动脉 ATP 输注和运动对腿部肌肉间隙 ATP 和去甲肾上腺素（NE）浓度的影响，以深入了解 ATP 引起肌肉血管舒张和交感神经节松解的间隙和血管内机制。在 10 名健康男性中，在 1）股动脉 ATP 输注（0.42 +/- 0.04 和 2.26 +/- 0.52 micromol/min；平均值 +/- SE）和 2）单腿伸膝运动（18 +/- 0 和 37 +/- 2 W）期间测量腿部血液动力学和肌肉间隙核苷酸和 NE 浓度。动脉 ATP 输注和运动分别使实验腿的腿部血流（LBF）从基线时的约 0.3 l/min 增加到 4.2 +/- 0.3 和 4.6 +/- 0.5 l/min，而对照腿的 LBF 减少或保持不变。在动脉 ATP 输注期间，两条腿的肌肉间隙 ATP、ADP、AMP 和腺苷浓度保持不变，但肌肉间隙 NE 从基线时的约 5.9 nmol/l 增加到实验腿和对照腿的 8.3 +/- 1.2 和 8.7 +/- 0.7 nmol/l（P < 0.05），同时动脉压降低（P < 0.05）。然而，在运动期间，收缩肌肉中间隙 ATP、ADP、AMP 和腺苷浓度增加（P < 0.05），但非活动肌肉中无变化，而 NE 浓度在活跃和非活跃肌肉中增加相似。这些结果表明，管腔内 ATP 的血管舒张和交感神经节松解作用主要通过内皮嘌呤能受体介导。管腔内 ATP 和肌肉收缩似乎通过抑制 NE 的作用而不是削弱其局部浓度来调节交感神经活性。
