People of Black African ethnicity (BA) have greater prevalence of hypertension than those of White European (WE) ethnicity and greater risk of developing hypertension-associated cardiovascular disease (CVD). Correspondingly, BAs show blunted flow-mediated dilatation of brachial artery and blunted forearm vasodilator responses to mental stress compared with WEs: decreased Nitric oxide (NO) availability has been implicated1,2. Prostaglandins (PGs) also contribute to endothelium-dependent dilatation, but their involvement in the forearm vasodilator response to mental stress, has not been explored in BAs, or WEs. Thus, we performed experiments on young recreationally-active BAs (18-26 years; n=9) and WEs (n=10), who were resident in the UK. Arterial blood pressure (ABP) was initially recorded by sphygmometry and continuously monitored by finger photoplethysmography. Forearm blood flow (FBF) was recorded at intervals by venous occlusion plethysmography; forearm vascular conductance (FVC) was calculated as FBF/ABP. Responses evoked following release of arterial occlusion for 2min (reactive hyperaemia) and by 5 sound stimuli: S1-5; 100dB, 2KHz, for 30s each at randomized intervals of 5-10min (mental stress), were recorded on 2 different days >2weeks apart, without or after the cyclooxygenase, inhibitor aspirin (600mg p.o). Without COX inhibition, mean ABP at baseline for the protocol was higher in BAs than WEs: 97±4.1 vs 78±3.3§ mmHg respectively (§: BA vs WE; P<0.05); after COX inhibition, mean ABP was 93±6.0 in BAs vs 82±3 mmHg in WEs. Baseline FVC was similar in WEs and BAs: 0.06±0.004 vs 0.05±0.01 conductance units (CU) respectively. However, reactive hyperaemia was greater in WEs than BAs and COX inhibition attenuated the peak change in FVC in WEs from 0.51±0.066 to 0.38±0.063* CU, but not in BAs: peak change in FVC 0.38±0.063§ vs 0.35±0.04 CU (*: before vs after aspirin; P<0.05). Without COX inhibition, WEs showed increases in FVC in response to S1-S5 and they were not affected by COX inhibition: +0.011±0.001 vs +0.019±0.013 at 15s in S1. By contrast, without COX inhibition, BAs showed an increases in FVC, but after COX inhibition S1-S5 evoked decreases in FVC indicating vasoconstriction: +0.017±0.001 vs -0.011±0.007 CU at 15s in S1. These results indicate that both reactive hyperaemia and forearm vasodilator response to mental stress are blunted in young BAs relative to WEs. We propose that vasodilator PGs make little contribution to the blunted reactive hyperaemia in BAs, but help preserve the forearm vasodilator response to mental stress in the face of reduced NO availability1. These characteristics may be early predictors of hypertension and CVD in BAs.