Women at altitude: Forearm hemodynamics during acclimatization to 4,300 m with α₁-adrenergic blockade

We hypothesized that blockade of α₁-adrenergic receptors would prevent the rise in peripheral vascular resistance that normally occurs during acclimatization. Sixteen eumenorrheic women were studied at sea level (SL) and at 4,300 m (days 3 and 10). Volunteers were randomly assigned to take the selective α₁-blocker prazosin or placebo. Venous compliance, forearm vascular resistance, and blood flow were measured using plethysmography. Venous compliance fell by day 3 in all subjects (1.39 ± 0.30 vs. 1.62 ± 0.43 ml·Δ30 mmHg^-1·100 ml tissue^-1·min^-1 at SL, means ± SD). Altitude interacted with prazosin treatment (P < 0.0001) such that compliance returned to SL values by day 10 in the prazosin-treated group (1.68 ÷± 0.19) but not in the placebo-treated group (1.20 ± 0.10, P < 0.05). By day 3 at 4,300 m, all women had significant falls in resistance (35.2 ± 13.2 vs. 54.5 ± 16.1 mmHg·ml^-1·min^-1 at SL) and rises in blood flow (2.5 ± 1.0 vs. 1.6 ± 0.5 ml·100 ml tissue^-1·min^-1 at SL). By day 10, resistance and flow returned toward SL, but this return was less in the prazosin-treated group (resistance: 39.8 ± 4.6 mmHg·ml^-1·min^-1 with prazosin vs. 58.5 ± 9.8 mmHg·ml^-1·min^-1 with placebo; flow: 1.9 ± 0.7 ml·100 ml tissue^-1·min^-1 with prazosin vs. 2.3 ± 0.3 ml·100 ml tissue^-1·min^-1 with placebo, P < 0.05). Lower resistance related to higher circulating epinephrine in both groups (r = -0.50, P < 0.0001). Higher circulating norepinephrine related to lower venous compliance in the placebo-treated group (r = -0.42, P < 0.05). We conclude that α₁-adrenergic stimulation modulates peripheral vascular changes during acclimatization.