Adenosine contributes to hypoxia-induced forearm vasodilation in humans. J. Appl. Physiol. 87(6): [2218][2219][2220][2221][2222][2223][2224] 1999.-In humans, hypoxia leads to increased sympathetic neural outflow to skeletal muscle. However, blood flow increases in the forearm. The mechanism of hypoxia-induced vasodilation is unknown. To test whether hypoxia-induced vasodilation is cholinergically mediated or is due to local release of adenosine, normal subjects were studied before and during

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... te hypoxia (inspired O 2 10.5%; ϳ20 min). In experiment I, aminophylline (50-200 µg · min Ϫ1 · 100 ml forearm tissue Ϫ1 ) was infused into the brachial artery to block adenosine receptors (n ϭ 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery (n ϭ 8). The responses of forearm blood flow (plethysmography) and forearm vascular resistance to hypoxia in the infused and opposite (control) forearms were compared. During hypoxia (arterial O 2 saturation 77 Ϯ 2%), minute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 Ϯ 6% in the control forearm but only by 5 Ϯ 8% in the aminophylline-treated forearm (P Ͻ 0.02). Accordingly, forearm vascular resistance decreased by 29 Ϯ 5% in the control forearm but only by 9 Ϯ 6% in the aminophylline-treated forearm (P Ͻ 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role. cholinergic vasodilation; aminophylline 8750-7587/99 $5.00