The current study aimed to determine whether acute hypoxia exposure in laboratory conditions associated with exercise induces an increase in systemic blood pressure (BP) in normotensive and hypertensive patients, and whether hypertensive patients are more prone to develop severe acute mountain sickness (sAMS). Finally, to determine if BP changes at exercise in acute hypoxia in hypertensive patients are predictive factors for sAMS. From 2012 to 2015, 852 normotensive and 106 hypertensive patients went through an acute hypoxia exercise test before a sojourn at high altitude. A subgroup of 228 normotensive was selected to match age, sex ratio, body weight and BMI and compared with the hypertensive group. In normotensive and hypertensive patients, for a given workload, BP was higher in hypoxia than in normoxia, whereas, for a given heart rate, it was lower in hypoxia than in normoxia. Hypertensive patients treated by beta-blockers showed lower arterial oxygen saturation (vs. other treatments) and blunted cardiac and ventilatory responses to hypoxia at exercise. Based on questionnaires filled out at high altitude, hypertensive patients were not more prone than normotensive patients to develop sAMS. During the laboratory acute hypoxic exercise test, hypertensive patients suffering from sAMS, although taking acetazolamide showed similar BP than hypertensive patients without sAMS and without acetazolamide. We hypothesize that acute hypoxia with exercise in laboratory conditions induces a peripheral vasodilation that balances vasoconstriction and tachycardia centrally induced through the adrenergic system. Hypertensive and normotensive patients behave similarly during exercise in acute hypoxia. Acute hypoxia does not exacerbate the exercise-induced increase in BP. BP variation, during the acute hypoxia exercise test, is not a useful predictor of intolerance to high altitude. Based on laboratory tests in acute hypoxia, hypertensive patients may not be at higher risk to develop sAMS at high altitude.