Mortensen Stefan P, Nyberg Michael, Thaning Pia, Saltin Bengt, Hellsten Ylva
Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen Ø, Denmark.
Hypertension. 2009 Jun;53(6):993-9. doi: 10.1161/HYPERTENSIONAHA.109.130880. Epub 2009 May 11.
Adenosine can induce vasodilation in skeletal muscle, but to what extent adenosine exerts its effect via formation of other vasodilators and whether there is redundancy between adenosine and other vasodilators remain unclear. We tested the hypothesis that adenosine, prostaglandins, and NO act in synergy to regulate skeletal muscle hyperemia by determining the following: (1) the effect of adenosine receptor blockade on skeletal muscle exercise hyperemia with and without simultaneous inhibition of prostaglandins (indomethacin; 0.8 to 1.8 mg/min) and NO (N(G)-mono-methyl-l-arginine; 29 to 52 mg/min); (2) whether adenosine-induced vasodilation is mediated via formation of prostaglandins and/or NO; and (3) the femoral arterial and venous plasma adenosine concentrations during leg exercise with the microdialysis technique in a total of 24 healthy, male subjects. Inhibition of adenosine receptors (theophylline; 399+/-9 mg, mean +/- SEM) or combined inhibition of prostaglandins and NO formation inhibited the exercise-induced increase in leg blood flow by 14+/-1% and 29+/-2% (P<0.05), respectively, but combined inhibition of prostaglandins, NO, and adenosine receptors did not result in an additive reduction of leg blood flow (31+/-5%). Femoral arterial infusion of adenosine increased leg blood flow from approximately 0.3 to approximately 2.5 L/min. Inhibition of prostaglandins or NO, or prostaglandins and NO combined, inhibited the adenosine-induced increase in leg blood flow by 51+/-3%, 39+/-8%, and 66+/-8%, respectively (P<0.05). Arterial and venous plasma adenosine concentrations were similar at rest and during exercise. These results suggest that adenosine contributes to the regulation of skeletal muscle blood flow by stimulating prostaglandin and NO synthesis.
腺苷可诱导骨骼肌血管舒张，但腺苷通过形成其他血管舒张剂发挥作用的程度以及腺苷与其他血管舒张剂之间是否存在冗余尚不清楚。我们通过确定以下内容来检验这一假设：腺苷、前列腺素和一氧化氮协同作用以调节骨骼肌充血，具体如下：（1）在有或没有同时抑制前列腺素（吲哚美辛；0.8至1.8毫克/分钟）和一氧化氮（N(G)-单甲基-L-精氨酸；29至52毫克/分钟）的情况下，腺苷受体阻断对骨骼肌运动性充血的影响；（2）腺苷诱导的血管舒张是否通过前列腺素和/或一氧化氮的形成介导；（3）使用微透析技术在总共24名健康男性受试者进行腿部运动期间测定股动脉和静脉血浆腺苷浓度。抑制腺苷受体（茶碱；399±9毫克，平均值±标准误）或联合抑制前列腺素和一氧化氮形成分别使运动诱导的腿部血流量增加减少了14±1%和29±2%（P<0.05），但联合抑制前列腺素、一氧化氮和腺苷受体并未导致腿部血流量进一步相加性减少（31±5%）。股动脉输注腺苷使腿部血流量从约0.3升/分钟增加至约2.5升/分钟。抑制前列腺素或一氧化氮，或联合抑制前列腺素和一氧化氮，分别使腺苷诱导的腿部血流量增加减少了51±3%、39±8%和66±8%（P<0.05）。静息和运动期间动脉和静脉血浆腺苷浓度相似。这些结果表明，腺苷通过刺激前列腺素和一氧化氮的合成来调节骨骼肌血流量。
