|Title:||Chronic hypoxia increases arterial blood pressure and reduces adenosine and ATP induced vasodilatation in skeletal muscle in healthy humans||Authors:||Calbet, J. A. L.
|UNESCO Clasification:||241106 Fisiología del ejercicio||Keywords:||Endothelium-Dependent Relaxation
Cellular Mechanisms, et al
|Issue Date:||2014||Publisher:||1748-1708||Journal:||Acta Physiologica||Abstract:||Aims:To determine the role played by adenosine, ATP and chemoreflexactivation on the regulation of vascular conductance in chronic hypoxia.Methods:The vascular conductance response to low and high doses ofadenosine and ATP was assessed in ten healthy men. Vasodilators wereinfused into the femoral artery at sea level and then after 8–12 days of res-idence at 4559 m above sea level. At sea level, the infusions were carriedout while the subjects breathed room air, acute hypoxia (FIO2=0.11) andhyperoxia (FIO2=1); and at altitude (FIO2=0.21 and 1). Skeletal muscleP2Y2 receptor protein expression was determined in muscle biopsies after4 weeks at 3454 m by Western blot.Results:At altitude, mean arterial blood pressure was 13% higher(91 2 vs. 102 3 mmHg,P<0.05) than at sea level and was unal-tered by hyperoxic breathing. Baseline leg vascular conductance was25% lower at altitude than at sea level (P<0.05). At altitude, the highdoses of adenosine and ATP reduced mean arterial blood pressure by 9–12%, independently of FIO2. The change in vascular conductance inresponse to ATP was lower at altitude than at sea level by 24 and38%, during the low and high ATP doses respectively (P<0.05), andby 22% during the infusion with high adenosine doses. Hyperoxicbreathing did not modify the response to vasodilators at sea level or ataltitude. P2Y2 receptor expression remained unchanged with altitude res-idence.Conclusions:Short-term residence at altitude increases arterial blood pres-sure and reduces the vasodilatory responses to adenosine and ATP.Keywordsadenosine, altitude, ATP, blood flow, chemoreflex.||URI:||http://hdl.handle.net/10553/50928||ISSN:||1748-1708||DOI:||10.1111/apha.12325||Source:||Acta Physiologica[ISSN 1748-1708],v. 211 (4), p. 574-584|
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