The central and peripheral vascular responses to acute mental stress (AMS) have been studied independently in a number of studies. Through this approach AMS has been shown to elicit vasodilation in the resistance beds of the forearm, but not the calf (Halliwill et al. 1997), and has been shown to increase aortic stiffness and pulse wave reflections (Vlachopoulos et al. 2006). Given the important role that vascular dysfunction plays in the development of risk factors for cardiovascular disease, it is perhaps surprising that concurrent measurement of central and peripheral vascular responses to AMS has not been reported. 10 healthy volunteers (5 male; age 27±2 yrs, height, 170±2cm; weight, 70±3 kg) underwent 10 minutes of baseline recordings before performing a six minute mental arithmetic task. Haemodynamic measurements were obtained using a non-invasive bio-impedance monitor (TaskForce Monitor). Radial artery pressure waveforms were acquired using applanation tonometry and central end-systolic pressure (ESP) was derived from the generated central waveforms using pulse wave analysis (Sphygmocor, AtCor Medical). Effective arterial elastance (EA), an index of arterial load, was calculated as ESP/stroke volume. Total peripheral resistance (TPR) was calculated as mean arterial pressure/cardiac output. In 5 subjects, brachial–radial pulse wave velocity (B-R PWV) was measured simultaneously and non-invasively by oscillometry (SciMed). In the remaining 5 subjects, forearm blood flow (FBF) was measured using strain gauge plethysmography. AMS increased FBF, and decreased TPR, confirming the expected vasodilatation of the peripheral vasculature. However, increased B-R PWV, and arterial load (EA), demonstrate increased conduit and central arterial stiffness during AMS. To our knowledge, these results provide the first concurrent measurements of differential vascular responses to AMS and they support a mechanistic link between AMS and increased risk factors for cardiovascular disease.