The contribution of prostaglandins (PGs) to exercise hyperaemia is controversial. However, most studies were performed on mixed groups of men and women and few mention ethnicity. BAs are at higher risk of developing hypertension relative to WEs; reduced endothelium-dependent dilatation is associated with hypertension. We hypothesised that young BAs show a blunted contribution of PGs to exercise hyperaemia compared to WEs, but the contribution of PGs is relatively preserved in young BA women by the facilitatory influences of oestrogen on endothelium. In 16 WEs and 19 BAs (10/6,11/8: M/F respectively, aged 18-29 years), we recorded changes in arterial pressure (ABP) by finger photoplethysmography and forearm blood flow (FBF) by venous occlusion plethysmography evoked by 2 min rhythmic handgrip exercise at 60% of maximum voluntary contraction before and after the COX inhibition with aspirin (600mg p.o). Values were compared by ANOVA. All subjects were recreationally active and normotensive (SP/DP <140/90mmHg). Resting FBF was similar in WEs and BAs (5.5±0.7 vs 5.6±0.4 ml/100ml tissue/min). Following rhythmic handgrip, FBF increased to 49.5±6.6* in WEs and 39.1±3.9* ml/100ml tissue/min in BAs (*: p<0.001 vs rest). The evoked increases in FBF were greater in WEs than BAs (P<0.05 WE vs BA). Further, within both ethnic groups, the increases in FBF were smaller in women: to 60.0±8.9 and 32.0±2.7§ ml/100ml tissue/min in WE men vs women (§: p<0.05 men vs women) and to 45.6 ±4.6 vs 28.9±5.4§ ml/100ml tissue/min in BA men and women. COX inhibition did not affect resting ABP, or FBF in WE or BA. However, the increases in FBF were attenuated in all WEs (49.5±6.6 vs 39.5±4.5† ml/100ml tissue/min: †: control vs aspirin) and all BAs (39.1±3.9 vs 33.9±3.8† ml/100ml tissue/min). Further COX inhibition attenuated the increases in forearm vascular conductance (FVC: FBF/ABP) in all WEs (to 0.57±0.05 vs 0.39±0.05† conductance units (CU)) and all BAs (0.40±0.04 vs 0.34±0.04† CU). However, whereas COX inhibition attenuated the increases in FVC in men in both ethnic groups (0.49±0.07 vs 0.35±0.06† in WEs and 0.42±0.07 vs 0.25±0.06† CU in BAs), it had no effect in women (WEs: 0.28±0.03 vs 0.20±0.02, P=0.09; BAs: 0.26±0.04 vs 0.29±0.04 CU, P=0.9) Thus, our results indicate that considered as mixed gender, young adult groups, BAs show attenuated exercise hyperaemia relative to WEs. Further, within both WEs and BAs, young women show blunted exercise hyperaemia relative to men. However, in contrast to our hypotheses, although the analysis of the full groups of BAs and WEs indicated PGs contribute to exercise hypeamia in both ethnicities, this largely reflects a substantial contribution of PGs to exercise hyperaemia in WE and BA men; any contribution of PGs to exercise hyperaemia is weak in both WE and BA women.