Calbet J A L, Boushel R, Robach P, Hellsten Y, Saltin B, Lundby C
Copenhagen Muscle Research Center, Rigshospitalet, Copenhagen, Denmark; Department of Physical Education, University of Las Palmas de Gran Canaria, Canary Islands, Spain; Research Institute of Biomedical and Health Sciences (IUIBS), Las Palmas de Gran Canaria, Canary Islands, Spain.
Acta Physiol (Oxf). 2014 Aug;211(4):574-84. doi: 10.1111/apha.12325. Epub 2014 Jun 30.
To determine the role played by adenosine, ATP and chemoreflex activation on the regulation of vascular conductance in chronic hypoxia.
The vascular conductance response to low and high doses of adenosine and ATP was assessed in ten healthy men. Vasodilators were infused into the femoral artery at sea level and then after 8-12 days of residence at 4559 m above sea level. At sea level, the infusions were carried out while the subjects breathed room air, acute hypoxia (FI O2 = 0.11) and hyperoxia (FI O2 = 1); and at altitude (FI O2 = 0.21 and 1). Skeletal muscle P2Y2 receptor protein expression was determined in muscle biopsies after 4 weeks at 3454 m by Western blot.
At altitude, mean arterial blood pressure was 13% higher (91 ± 2 vs. 102 ± 3 mmHg, P < 0.05) than at sea level and was unaltered by hyperoxic breathing. Baseline leg vascular conductance was 25% lower at altitude than at sea level (P < 0.05). At altitude, the high doses of adenosine and ATP reduced mean arterial blood pressure by 9-12%, independently of FI O2 . The change in vascular conductance in response to ATP was lower at altitude than at sea level by 24 and 38%, during the low and high ATP doses respectively (P < 0.05), and by 22% during the infusion with high adenosine doses. Hyperoxic breathing did not modify the response to vasodilators at sea level or at altitude. P2Y2 receptor expression remained unchanged with altitude residence.
Short-term residence at altitude increases arterial blood pressure and reduces the vasodilatory responses to adenosine and ATP.
确定腺苷、三磷酸腺苷（ATP）和化学反射激活在慢性低氧时对血管传导调节中所起的作用。
评估了10名健康男性对低剂量和高剂量腺苷及ATP的血管传导反应。血管扩张剂在海平面时注入股动脉，然后在海拔4559米处居住8 - 12天后再次注入。在海平面时，注入血管扩张剂是在受试者呼吸室内空气、急性低氧（吸入氧分数=0.11）和高氧（吸入氧分数=1）的情况下进行；在海拔高度时（吸入氧分数=0.21和1）。通过蛋白质印迹法测定在海拔3454米处居住4周后肌肉活检中骨骼肌P2Y2受体蛋白表达。
在海拔高度时，平均动脉血压比海平面时高13%（91±2对102±3 mmHg，P<0.05），且高氧呼吸对其无影响。海拔高度时腿部血管传导基线比海平面时低25%（P<0.05）。在海拔高度时，高剂量的腺苷和ATP使平均动脉血压降低9 - 12%，与吸入氧分数无关。在低剂量和高剂量ATP时，海拔高度时对ATP的血管传导变化分别比海平面时低24%和38%（P<0.05），在高剂量腺苷注入时低22%。高氧呼吸在海平面或海拔高度时均未改变对血管扩张剂的反应。随着海拔居住时间的延长，P2Y2受体表达保持不变。
短期居住在海拔高度会增加动脉血压，并降低对腺苷和ATP的血管舒张反应。
