The prevalence of cardiovascular disease (CVD) is greater in South Asians (SAs) than White Europeans (WEs). Oestrogen is generally considered to protect against CVD; it facilitates the dilator influences of nitric oxide (NO) and cyclooxygenase (COX) products (prostaglandins: PGs). However, there is evidence the prevalence of hypertension is greater in SA than WE women1 and that SA women have greater risk of coronary artery disease, present at an earlier age and have higher risk of mortality2. Whether markers of CVD can be recognised in young SA women is unknown. Thus, in 12 SA and 12 WE women (18-26 years old), we compared endothelium-dependent vasodilator responses evoked in forearm cutaneous circulation by iontophoresis of acetylcholine (ACh; 7 pulses at 0.1mA followed by 1 pulse at 0.2mA for 30s each at 1 min intervals) and following release of arterial occlusion for 2 min (the reactive hyperaemia), by using laser Doppler fluximetry to continuously record cutaneous red cell flux in perfusion units (pu). All women were normotensive (SP/DP < 140/90 mmHg) and non-diabetic. All were tested in the early follicular phase of the menstrual cycle when oestrogen is low. Under control conditions, both responses were blunted in SA relative to WE women: average ACh responses were +230±25 vs 134±20* (*: P< 0.05 2-way ANOVA WE vs SA), while peak reactive hyperaemia was +98±11 vs 57±10*pu. After topical application of the NO synthase inhibitor L-NAME (100nM for 30min), ACh-evoked dilatation and reactive hyperaemia were attenuated in WE women (161±16§pu and 65±7§pu; §: P<0.01, paired t-test vs control), but not in SA women (104±11 pu and 48±8 pu; P>0.05). Similarly, 30 min after the COX inhibitor aspirin (600 mg p.o.), ACh-evoked dilatation was attenuated in WE women (155±18§pu) while peak reactive hyperaemia was 73±14pu; p=0.06 vs control), whereas neither ACh-evoked dilatation, nor reactive hyperaemia were significantly altered in SA women (123±20 and 63±10 pu respectively). Finally, with dual NO synthase and COX inhibition, ACh-evoked dilatation and reactive hyperaemia were similar to control responses in WE women (208±19 and 74±11pu respectively) and in SA women, but they were blunted in SA relative to WE women (117±19* and 50±8*pu respectively). These results suggest that in young adult SA women with no overt CVD, endothelium-dependent dilatation is blunted relative to that of young WE women and this can be attributed to attenuated contributions of NO and vasodilator PGs in SA women. Further, assuming responses evoked in the presence of COX and NOS inhibition reflect the influences of endothelium-derived hyperpolarising factor (EDHF), it seems these influences are substantial in both WE and SA women, but are also blunted in young SA women. We propose the protective influences of oestrogen on endothelium-dependent dilatation may be deficient in young SA women and explain their increased risk of CVD.