Adenosine contributes to hypoxia-induced forearm vasodilation in humans

In humans, hypoxia leads to increased sympathetic neural outflow to skeleta l muscle. However, blood Slow increases in the forearm. The mechanism of hy poxia-induced vasodilation is unknown. To test whether hypoxia-induced vaso dilation is cholinergically mediated or is due to local release of adenosin e, normal subjects were studied before and during acute hypoxia (inspired O -2 10.5%; similar to 20 min). In experiment I, aminophylline (50-200 mu g.m in(-1).100 ml forearm tissue(-1)) was infused into the brachial artery to b lock adenosine receptors (n = 9). In experiment II, cholinergic vasodilatio n was blocked by atropine (0.4 mg over 4 min) infused into the brachial art ery (n = 8). The responses of forearm blood Slow (plethysmography) and fore arm vascular resistance to hypoxia in the infused and opposite (control) fo rearms were compared. During hypoxia (arterial O-2 saturation 77 +/- 2%), m inute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 +/- 6% in the control forearm but only by 5 +/- 8% in the aminophylline-treated forearm (P < 0.02). Accordin gly, forearm vascular resistance decreased by 29 +/- 5% in the control fore arm but only by 9 +/- 6% in the aminophylline-treated forearm (P < 0.02). A tropine did not attenuate forearm vasodilation during hypoxia. These data s uggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.