We previously demonstrated a bimodal distribution of forearm vasodilator responsiveness to adenosine (ADO) infusion in the brachial arteries of human subjects. We also demonstrated that ADO receptor antagonism blunted exercise hyperaemia during heavy rhythmic handgripping, but vasodilator responses to exogenous ADO were only blunted in ADO responders. In this study, we continued investigating the contribution of ADO to exercise hyperaemia and possible differences between responders and nonresponders. We hypothesized that ADO transporter antagonism would increase vasodilatation to exogenous ADO in responders only, but not effect exercise-mediated vasodilation. To test this hypothesis, we compared forearm vascular conductance (FVC) during infusion of ADO to FVC during handgripping before and after infusion of dipyridamole (DIP) in 20 subjects. In ADO responders, change in FVC above baseline (ml min^-1 100mmHg^-1) for low, medium, and high doses of ADO, respectively, was 58±8, 121±22, 184±38, and after DIP was 192±32, 238±50, and 310±79. For nonresponders, these values were 23±2, 43±5, 66±9 before DIP (P < 0.01 vs. responders). In contrast to our hypothesis, these values were increased by DIP in nonresponders (P < 0.001) and, therefore, not different from responders (P > 0.20). We found that ADO transporter blockade had no effect on exercise hyperaemia in either subgroup. We conclude that there may be increased ADO transporter activity in nonresponders resulting in reduced ADO-mediated vasodilatation. The failure of DIP to augment exercise hyperemia under these conditions suggests that ADO concentrations may not rise enough during rhythmic handgripping to have a major impact on these responses.