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

Abstract

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 10in 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−1at 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.