Martin, Élizabeth

We previously demonstrated a bimodal distribution of vasodilator responsiveness to adenosine (ADO) infusion in human subjects: one subgroup demonstrated robust vasodilator responses to ADO (ADO responders) and the other showed blunted responses (non‐responders). Furthermore, ADO receptor antagonism blunted ADO vasodilator responses only in ADO responders and blunted exercise vasodilation only at high workloads in both groups. To test the hypothesis that ADO transporter antagonism would augment vasodilator responsiveness to ADO and exercise only in ADO responders, we compared forearm vasodilation to intra‐arterial infusion of three doses of ADO to vasodilation during three workloads of forearm handgrip exercise before and after ADO transporter antagonism with dipyridamole (DYP) in 10 subjects. In ADO responders (n=5), the change in forearm vascular conductance above baseline (ml min −1 100mmHg −1 ) for the low, medium, and high doses of ADO, respectively, was 61 ± 15, 117 ± 35, 164 ± 47 before DYP and 160 ± 50, 171 ± 59, and 216 ± 87 after DYP. For non‐responders (n=5), these values were 20 ± 2, 36 ± 6, 57 ± 14 before DYP ( P < 0.05 vs. responders) and were 159 ± 40, 293 ± 53, and 377 ± 82 after DYP ( P > 0.05 vs. responders). ADO transporter blockade had no effect on exercise hyperemia in either group ( P > 0.05 for pre vs. post‐DYP). We conclude that there may be increased ADO transporter activity in non‐responders resulting in increased clearance of ADO from the interstitium and that, in both subgroups, ADO is not obligatory for exercise hyperemia.