SYSTEMIC HYPERTENSION AT 4,300 M IS RELATED TO SYMPATHOADRENAL ACTIVITY

Residence at high altitude has been associated with elevation in systemic arterial blood pressure, but the time course has been little studied and the mechanism is unknown. Because plasma epinephrine (E) and norepinephrine (NE) also increase at altitude, we hypothesized that heightened sympathoadrenal activity may cause increased arterial pressure. We measured ambulatory blood pressure by cuff monitor in relation to 24-h urinary excretion of E and NE at sea level and during 3 wk of residence at 4,300 m (Pikes Peak, CO) in 11 healthy men. In five subjects taking placebo, arterial pressure progressively increased at 4,300 m from 82 +/- 1 (SE) mmHg at sea level to 88 +/- 3 on day 2, 91 +/- 3 on day 8, and 97 +/- 6 on clay 17. In six subjects, propranolol (240 mg/day) decreased pressure from 85 +/- 4 to 77 +/- 1 mmHg at sea level but did not prevent sustained increase in pressure at 4,300 m (84 +/- 1, 81 +/- 1, and 85 +/- 3 mmHg on clays 2, 8, and 17, respectively). Compared with the placebo group, blood pressure did not increase further over the inital elevation observed on day 2 in the propranolol group. There was interindividual variability in the blood pressure responses in both groups, with some subjects demonstrating a more marked increase in blood pressure. Urinary excretion of NE increased concomitantly with pressure at altitude in both groups, with a greater rise in the placebo group. Blood pressures were related to NE excretion in the placebo (r = 0.67, P < 0.005) and propranolol groups (r = 0.47, P < 0.05), and subjects with the highest blood pressures at 4,300 m had the greatest NE values. Mean urinary E levels did not increase over time in the placebo group and increased only minimally at day 17 in the propranolol group. Despite this lack of increase in E at 4,300 m, arterial pressure was related to urinary E levels in the placebo (r = 0.75, P < 0.005) but not the propranolol group. Thus, elevation in systemic arterial pressure at 4,300 m was related to increased sympathetic activity from NE. The possibility that E also contributed to the rise in arterial pressure could not be excluded.