Women at altitude: forearm hemodynamics during acclimatization to 4,300 m with alpha(1)-adrenergic blockade

• Published in: American journal of physiology. Heart and circulatory physiology 2001-12, Vol.281 (6), p.H2636-H2644
• Main Authors: Zamudio, S, Douglas, M, Mazzeo, R S, Wolfel, E E, Young, D A, Rock, P B, Braun, B, Muza, S R, Butterfield, G E, Moore, L G
• Format: Article
• Language: English
• Subjects: Acclimatization - drug effects; Acclimatization - physiology; Adrenergic alpha-Antagonists - pharmacology; Adult; Altitude; Blood Pressure - drug effects; Blood Pressure - physiology; Epinephrine - blood; Female; Forearm - physiology; Humans; Norepinephrine - blood; Plethysmography; Prazosin - pharmacology; Regional Blood Flow - drug effects; Regional Blood Flow - physiology; Space life sciences; Vascular Resistance - drug effects; Vascular Resistance - physiology; Veins - physiology
• ISSN: 0363-6135
• DOI: 10.1152/ajpheart.2001.281.6.H2636

We hypothesized that blockade of alpha(1)-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 alpha(1)-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. Delta 30 mmHg(-1) x 100 ml tissue(-1) x 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 x ml(-1) x min(-1) at SL) and rises in blood flow (2.5 +/- 1.0 vs. 1.6 +/- 0.5 ml. 100 ml tissue(-1) x 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 x ml(-1) x min(-1) with prazosin vs. 58.5 +/- 9.8 mmHg x ml(-1) x min(-1) with placebo; flow: 1.9 +/- 0.7 ml. 100 ml tissue(-1) x min(-1) with prazosin vs. 2.3 +/- 0.3 ml x 100 ml tissue(-1) x 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 alpha(1)-adrenergic stimulation modulates peripheral vascular changes during acclimatization.