Journal of Applied Physiology
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J Appl Physiol 87: 2218-2224, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 6, 2218-2224, December 1999

Adenosine contributes to hypoxia-induced forearm vasodilation in humans

Urs A. Leuenberger, Kris Gray, and Michael D. Herr

Section of Cardiology, Department of Medicine, The Milton S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033

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 acute hypoxia (inspired O2 10.5%; ~20 min). In experiment I, aminophylline (50-200 µg · min-1 · 100 ml forearm tissue-1) was infused into the brachial artery to block adenosine receptors (n = 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery (n = 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 O2 saturation 77 ± 2%), minute 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). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the aminophylline-treated forearm (P < 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


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