The Roles of Nitric Oxide in Dilating Proximal and Terminal Arterioles of Skeletal Muscle during Systemic Hypoxia

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Abstract
Indirect evidence suggests that dilatation evoked by systemic hypoxia in proximal and terminal arterioles of skeletal muscle is mediated by adenosine acting on A1 receptors, but that the dilatation of proximal arterioles requires the presence of nitric oxide (NO), whereas that of terminal arterioles is mediated by NO. In the present study, we showed that primary and terminal arterioles of spinotrapezius muscle (diameters: 45 ± 4 and 9 ± 1 µm, respectively) in anaesthetised rats dilated by 15 ± 7 and 48 ± 24%, respectively, during hypoxia (breathing 12% O2). Inhibition of NO synthesis with intravenous nitro-L-arginine methyl ester attenuated these responses (to –2 ± 3 and –4 ± 4%, respectively). However, when a tonic level of NO was subsequently restored by infusion of NO donor, hypoxia evoked dilatation of primary arterioles (+24 ± 8%) but not terminal arterioles (0 ± 4%). The adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) (intravenous) attenuated this ‘restored’ primary arteriolar vasodilatation (to +6 ± 3%). Similar results were obtained with 8% O2. We propose that (1) proximal arteriolar dilatation evoked by systemic hypoxia depends on a background level of NO, which facilitates the action of adenosine on A1 receptors, and (2) hypoxia-evoked dilatation of terminal arterioles is mediated by NO synthesised via A1 receptor stimulation.