Orthostatic Tolerance During al Adrenergic Receptor Blockade at High Altitude.

In the first two weeks of high altitude (HA) exposure, blood pressure typically rises due, in part, to a large increase in sympathetic stimulation. We hypothesized that blocking al-adrenergic receptors would impair circulatory compensation to an orthostatic challenge to a greater extent at HA than at sea level (SL). Sixteen healthy women (23 +/- 2 yr) were randomly assigned to receive either 2 mg prazosin (n = 8) or placebo (n = S) t.i.d. (double-blind design) for 12 d at SL and during the first 12 d of HA residence (4300 m). Passive &)O upright tilt was performed at SL (10 d of treatment), and after 3 and 10 d at HA. Mean arterial blood pressure (MBP, auscultation) and heart rate (HR, ECG) were measured every min during 10 min each of supine rest and tilt. For the prazosin group compared to the placebo group: (1) At SL, supine and tilt MBP were lower (P < 0.05) and, at HA, MBP was lower only in the first several min of tilt on day 10 (P <0.05); (2) At SL or HA, HR was similar for either position; and (3) From supine to tilt, the drop in MBP was greater only at SL and the increase in HR was consistently greater only at HA (both P < 0.05). We conclude that al-adrenergic blockade altered MBP and HR responses to tilt at SL and HA, but that orthostatic tolerance was well maintained in both environments. Compensatory adjustments were likely in either sympathetic and parasympathetic neural discharge or in other receptor activities.