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Measurement of nitric oxide release evoked by systemic hypoxia and adenosine from rat skeletal muscle in vivo

Ray, Clare J. ; Marshall, Janice M.

The Journal of physiology, 2005-11, Vol.568 (3), p.967-978 [Periódico revisado por pares]

9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society

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  • Título:
    Measurement of nitric oxide release evoked by systemic hypoxia and adenosine from rat skeletal muscle in vivo
  • Autor: Ray, Clare J. ; Marshall, Janice M.
  • Assuntos: Adenosine - metabolism ; Animals ; Hypoxia - metabolism ; Male ; Muscle, Skeletal - blood supply ; Muscle, Skeletal - metabolism ; Nitric Oxide - blood ; Nitric Oxide Synthase - metabolism ; Rats ; Rats, Wistar ; Receptor, Adenosine A1 - metabolism ; Tissue, System and Organ Physiology
  • É parte de: The Journal of physiology, 2005-11, Vol.568 (3), p.967-978
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
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  • Descrição: It is accepted that NO plays a role in hypoxic vasodilatation in several tissues. For rat hindlimb muscle there is evidence that during systemic hypoxia endogenously released adenosine acts on endothelial A 1 receptors to evoke dilatation in a NO-dependent fashion, implying requirement for, or mediation by, NO. We tested in vivo whether systemic hypoxia and adenosine release NO from muscle. In anaesthetized rats, arterial blood pressure (ABP) and femoral blood flow (FBF) were recorded allowing computation of femoral vascular conductance (FVC). Blood samples taken from femoral artery and vein allowed electrochemical measurement of plasma [NO] after reduction of NO 3 − and NO 2 − . Systemic hypoxia and adenosine infusion for 5 min each, evoked an increase in FVC that was attenuated by the NO synthase (NOS) inhibitor l -NAME (Group 1, n = 8) and adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, Group 2, n = 6). Concomitant systemic hypoxia and adenosine infusion evoked increases in venous–arterial [NO] difference ([NO] v-a ) from −1.4 ± 0.85 to 6.6 ± 1.6 and 2.3 ± 0.78 to 8.4 ± 1.8 nmol l −1 , respectively (mean ± s.e.m ), which were abolished by l -NAME (−0.72 ± 0.90 to −0.87 ± 0.74 and 0.72 ± 0.85 to −0.97 ± 1.1 nmol l −1 , respectively). DPCPX also abolished the hypoxia-evoked increase in [NO] v-a (control −4.2 ± 1.8 to 12.5 ± 3.7 nmol l −1 , with DPCPX −0.63 ± 2.6 to 3.3 ± 2.9 nmol l −1 ) and decreased the adenosine-evoked increase in [NO] v-a (control 1.1 ± 1.5 to 24 ± 14, with DPCPX −0.43 ± 2.9 to 12 ± 5.9 nmol l −1 ). These results allow the novel conclusion that the muscle vasodilatation of systemic hypoxia is partly mediated by adenosine acting at endothelial A 1 receptors to stimulate synthesis and release of NO, which then induces dilatation.
  • Editor: 9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society
  • Idioma: Inglês
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