Sodium regulating hormones at high altitude: basal and post-exercise levels.

High altitude (HA)-induced diuresis is associated with marked changes in sodium and water regulating hormones, particularly the renin-angiotensin-aldosterone system (RAAS) and atrial natriuretic hormone (ANH). These hormones are also strongly stimulated by physical exercise, which is a major component of daily activity at HA. In spite of the numerous studies in literature, a clear relationship between hormonal changes, HA diuresis, and physical exercise has not yet been established. We therefore evaluated the response of sodium regulating hormones to exhaustive exercise in a group of seven males exposed to prolonged HA hypoxia. The study was divided into four phases: sea level (SL1), after 7 (P1) and after 21 (P2) days at 5050 m (Italian National Research Council Pyramid Laboratory, Nepal), and back at sea level (SL2). At each phase plasma hematocrit (Ht), total body water (TBW), 24-hr sodium excretion (uNa), and urinary volume (uV) were evaluated together with PRA, plasma aldosterone, and ANH, in samples drawn basally from patients in upright position, and at the end of graded step-wise (30 W/2 min) maximal exercise. Levels of uNa and uV were raised at P1 and then declined at P2, with a parallel decrease in TBW and an increase in Ht. Basal PRA and aldosterone levels were suppressed both at P1 and P2 (from 1.9 +/- 0.4 to 0.08 +/- 0.03 and 0.5 +/- 0.1 ng/mL/3 h, and from 7.9 +/- 1.8 to 3.9 +/- 0.4 and 4.5 +/- 0.4 ng/dL, respectively; P < .05). Exhaustive exercise at HA did not induce any significant response in PRA and aldosterone, unlike SL1. Otherwise at P1 ANH levels remained unchanged both basally and during exercise, while at P2 they decreased significantly vs. SL1, both basally and after exercise (from 13.3 +/- 5.7 to 3.5 +/- 1.2 and from 40.2 +/- 10.2 to 17.5 +/- 8.3, respectively; P < .05). Our data show that PRA and aldosterone levels were constantly suppressed at HA and were unresponsive to exercise, whereas the ANH response was significantly stimulated during acute HA exposure, but not during chronic exposure. This suggests that hypoxia-induced chemoreceptor stimulation may cause the natriuretic phenomenon through direct suppression of the RAAS.