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

Citation
Ee. Wolfel et al., SYSTEMIC HYPERTENSION AT 4,300 M IS RELATED TO SYMPATHOADRENAL ACTIVITY, Journal of applied physiology, 76(4), 1994, pp. 1643-1650
Citations number
24
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
4
Year of publication
1994
Pages
1643 - 1650
Database
ISI
SICI code
8750-7587(1994)76:4<1643:SHA4MI>2.0.ZU;2-I
Abstract
Residence at high altitude has been associated with elevation in syste mic arterial blood pressure, but the time course has been little studi ed and the mechanism is unknown. Because plasma epinephrine (E) and no repinephrine (NE) also increase at altitude, we hypothesized that heig htened 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 res idence 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 bu t 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). Com pared 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 increas e in blood pressure. Urinary excretion of NE increased concomitantly w ith pressure at altitude in both groups, with a greater rise in the pl acebo group. Blood pressures were related to NE excretion in the place bo (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 great est NE values. Mean urinary E levels did not increase over time in the placebo group and increased only minimally at day 17 in the propranol ol group. Despite this lack of increase in E at 4,300 m, arterial pres sure was related to urinary E levels in the placebo (r = 0.75, P < 0.0 05) but not the propranolol group. Thus, elevation in systemic arteria l pressure at 4,300 m was related to increased sympathetic activity fr om NE. The possibility that E also contributed to the rise in arterial pressure could not be excluded.