LAUSR

Heterogeneous flow-mediated dilation (FMD) and low-flow-mediated constriction (L-FMC) responses have been reported between upper- and lower-limb arteries. Radial artery L-FMC, but not FMD, responses are blunted when endothelial-derived hyperpolarizing factors (EDHF) or prostaglandin production are inhibited in young adults. However, it is unknown if these mechanisms similarly impact endothelial-dependent responses in the brachial (BA) and popliteal (POP) arteries. We tested the hypotheses that BA-L-FMC and POP-L-FMC would be attenuated following independent EDHF and prostaglandin inhibition. Eighteen participants (23 ± 3years; 6♀) completed 3 randomized and double-blinded ultrasound assessments following ingestion of an opaque capsule containing maltodextrin (Control), 150mg Fluconazole (EDHF inhibition) or 500mg Aspirin (prostaglandin inhibition). POP resting diameter was reduced following Fluconazole administration (6.13±0.63 mm versus 6.19±0.65 mm in Control, P=0.03). Compared to Control, Fluconazole also blunted the relative L-FMC responses in both the BA (-2.1 ± 0.8% versus -0.8 ± 1.0%, P=0.001) and POP (-1.7±1.1% versus -0.8±0.9%, P=0.009). In contrast, Aspirin did not impact either the BA (-1.9±0.7%) or POP-L-FMC (-1.3±0.6%) responses (both, P>0.35). The FMD response was unchanged following Fluconazole or Aspirin administration in either artery (both, P>0.36). Our findings demonstrate that EDHF mediates L-FMC responses in both the brachial and popliteal arteries. Complementary to the nitric oxide-mediated FMD response, L-FMC appears to provide information regarding the EDHF pathway. Future research should uncover if these mechanisms impact older adults and/or patient populations characterized by vascular endothelial dysfunction associated with low aerobic fitness and habitual physical activity levels.