Background: Increased blood level of norepinephrine, a primary α-adrenergic agonist, is associated with high-altitude exposure, and may help regulate key physiological functions (e.g., blood pressure). We hypothesized that blocking α1-adrenergic receptors would impair circulatory compensation for an orthostatic challenge to a greater extent at altitude than at sea level. Methods: Sixteen healthy women (23 ± 2 yr) were randomly assigned to receive either 2 mg prazosin (n = 8) or placebo (n = 8) t.i.d. (double-blind design) for 12 d at sea level and during the first 12 d of altitude residence (4300 m). Passive 60° upright tilt was performed at sea level (10 d of treatment), and after 3 and 10 d at altitude. Mean arterial BP (MABP, via auscultation) and heart rate (HR, via ECG) were measured every min during 10 min each of supine rest and tilt. Results: For the prazosin group compared with the placebo group: 1.) Supine and tilt MABP were consistently lower (p < 0.05) at sea level; 2.) MABP did not differ (p > 0.05) for either day at altitude; 3.) HR was similar for both positions at sea level and altitude; and 4.) MABP was consistently less only at sea level and HR was consistently greater only at altitude (both p < 0.05) in response to tilt. Conclusions: α1-adrenergic blockade altered MABP and HR responses to tilt at sea level and altitude, but circulatory responses to orthostasis were well maintained in both environments. At altitude, BP during tilt was sufficiently maintained by a compensatory increase in heart rate, likely mediated by parasympathetic withdrawal.
|Number of pages||6|
|Journal||Aviation Space and Environmental Medicine|
|State||Published - 11 Dec 2001|
- Parasympathetic withdrawal
- Sympathetic nervous system
- α-Adrenergic receptors