Altitude-induced hypoxia is related to functional adaptations including tachycardia and hypertension. Aim of this study was to evaluate urinary excretion of different biochemical pressure mediators in eight mountain climbers staying at an altitude ranging from 2000 and 5150 metres above sea level for 6 days. Blood pressure, heart rate, blood oxygen saturation were recorded at rest in pre-hypoxic conditions (sea level), in hypoxic conditions (at 4000 m altitude, soon after 3 days acute exposure at 4000–5150 m altitude) and in post-hypoxic conditions (sea level). Urinary samples were obtained in pre-hypoxic, hypoxic and post-hypoxic conditions, stored at ­20 °C and finally assayed by radioimmunoassay for 8-iso-PGF2a, HPLC-EC for norepinephrine and epinephrine, and HPLC-UV for ADMA and creatinine determination. Blood oxygen saturation at high altitude (4000 m) was significantly lower compared to sea level (P<0.05); on the other hand, compared to sea level, heart rate and (systolic-diastolic) blood pressure were significantly higher at high altitudes, both (P<0.05). Urinary epinephrine, norepinephrine, 8-iso-PGF2a and ADMA were significantly higher at high altitudes, both (P<0.01), and returned to basal levels soon after returning to sea level. 3 days hypoxic exposure at high altitude (4000–5150 m) temporarily stimulated blood pressure possibly by enhancing the production of pressure mediators such as catecholamines, 8-iso-PGF2a and ADMA. In particular, our work shows, in humans, a direct correlation between ADMA excretion and blood pressure during high altitude exposure, pointing to a possible involvement of ADMA in transient hypertension induced by exposure to hypoxia.