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1 Anesthesiology, Mayo College of Medicine, Rochester, Minnesota, United States; Physiology and Biomedical Engineering, Mayo College of Medicine, Rochester, Minnesota, United States
* To whom correspondence should be addressed. E-mail: martin.elizabeth2{at}mayo.edu.
To gain insight into the role of adenosine in exercise hyperemia, we compared forearm vasodilation induced by intra-arterial infusion of three doses of adenosine (ADO) to vasodilation during three workloads of handgrip exercise in 27 human subjects. We measured forearm blood flow using Doppler ultrasound and calculated forearm vascular conductance (FVC). We found that about half of the subjects demonstrated robust vasodilator responsiveness to both ADO infusion and exercise, and the other half demonstrated blunted vasodilator responsiveness to ADO infusion compared to exercise. In 15 subjects ("ADO responders"), the change in FVC above baseline (ml min-1 100 mmHg-1) was 209±33, 419±57, 603±75 for the low, medium, and high doses of ADO, respectively, and 221±35, 413±54, 582±70 for the low, medium, and high exercise workloads, respectively. In the other 12 subjects ("ADO non-responders"), the change in FVC above baseline was 102±36, 113±42, 151±54 for the low, medium, and high doses of ADO, respectively (P < 0.05 vs. ADO responders), whereas exercise hyperemia was not different from ADO responders (P > 0.05). Furthermore, infusion of NG-monomethyl-L-arginine (L-NMMA) blunted vasodilator responses to ADO infusion only in ADO responders (P < 0.01 vs. post-L-NMMA) and had no effect on exercise in either group. Responses to reactive hyperemia were not different between subgroups. We conclude that vasodilator responsiveness to ADO exhibits a bimodal distribution among human subjects involving differences in the contribution of nitric oxide to ADO-mediated vasodilation. Finally, our data support the concept that neither ADO nor nitric oxide is obligatory for exercise hyperemia.
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