Effects of prolonged high-altitude exposure on peripheral adrenergic receptors in young healthy volunteers

The regulation of adrenergic receptors during hypoxia is complex, and the r esults of published reports have not been consistent. In the present study blood cell adrenoceptor characteristics at sea level (SL) before and after prolonged exposure to high altitude (HA) were measured in seven trained you ng male lowlanders. Sympathoadrenal activity and clinical haemodynamic para meters were also evaluated before departure (SLB), after 1 week (HA1) and 4 weeks (HA4) at HA and 1 week after return to sea level (SLA). As compared to pre-departure sea level values, urinary norepinephrine excretion increas ed significantly during altitude exposure [SLB: 10.26 (3.04) mu g . 3 h(-1) ; HA1: 23.2 (4.19) mu g . 3 h(-1); HA4: 20.3 (8.68) mu g . 3 h(-1)] and fel l to pre-ascent values 1 week after return to sea level [SLA: 9 (2.91) mu g . 3 h(-1)]. In contrast, mean urinary epinephrine levels did not increase o ver time at HA. Both systolic and diastolic blood pressures, as well as hea rt rate, were increased during HA exposure. The circadian blood pressure an d heart rate rhythms were preserved during all phases of altitude exposure. Mean maximal binding (B-max) of the alpha(2)-adrenoceptor antagonist [H-3] rauwolscine to platelet membranes was significantly reduced (P < 0.001) aft er exposure to chronic hypoxia [SLB: 172.6 (48.5) fmol . mg(-1) protein ver sus SLA: 136.8 (56.1) fmol . mg(-1) protein] without change in the dissocia tion constant (K-D). Neither the lymphomonocyte beta(2)-adrenoceptor B-max [SLB: 38.5 (13.6) fmol . mg(-1) protein, versus SLA: 32.4 (12.1) fmol . mg( -1) protein] nor the K-D for [H-3]dihydroalprenolol was affected by chronic hypoxia. Cyclic AMP (adenosine 3',5'-cyclic monophoshate) generation in ly mphomonocytes by maximal isoproterenol stimulation was not modified after p rolonged HA exposure. In conclusion, the downregulation of alpha(2)-adrenoc eptors appears to be an important component of the adrenergic system respon se to HA exposure.