The hemodynamic and autonomic mechanisms underlying post-exercise hypotension (PEH) in hypertensives are not firmly established. This study aimed at investigating the interplay of neural and hemodynamic mechanisms involved in PEH in hypertension. In 15 middle-age subjects with mild essential hypertension, we evaluated before and after maximal exercise: Blood Pressure (BP), Cardiac Output (CO), Total Peripheral Resistances (TPR), Forearm (FVR) and Calf (CVR) vascular resistances, and autonomic function [by spectral analysis of RR-interval and BP variabilities and spontaneous baroreflex sensitivity (BRS)]. Systolic and diastolic BP were significantly reduced from baseline 60 to 90 min after exercise. TPR was significantly reduced as was CVR, whereas CO and FVR were unchanged. HR was also unchanged. The low frequency (LF) component of BP variability increased significantly after exercise, whereas the LF component of RR-interval variabilty was unchanged. Overall change in BRS was not significant after exercise with respect to baseline, although a significant, albeit small, increase in BRS was observed in response to hypotensive stimuli. These findings indicate that in hypertensive patients, post-exercise hypotension is mediated mainly by a peripheral vasodilation, which may involve metabolic factors linked to postexercise hyperemia in the active limbs. The vasodilator effect appears to override a concomitant, reflex sympathetic activation selectively directed to the vasculature, possibly aimed to oppose excessive BP decreases. Finally, the cardiac component of arterial baroreflex is reset during the hypotension following exercise, although the baroreflex mechanisms controlling heart period appear to retain the potential for a greater opposition to hypotensive stimuli.