Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

Abstract

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.

Acetazolamide and chronic hypoxia: effects on haemorheology and pulmonary haemodynamics

“…Therefore, one may suggest that the decrease in Hct in hypoxic rats treated by acetazolamide was not fully explained by the decrease in erythropoiesis (as suggested by the decrease in percentage of reticulocytes), and was also probably the resulting effect of the plasma volume rise, which could be interpreted as a physiological adaptation for maintaining blood volume at the normal value. The hypoxia-induced decrease in plasma volume was probably attributed to the well-known blunting effect of hypoxia on the renin-aldosterone system [21] and other complex mechanisms, such as peripheral arterial chemoreception [23,24]. The mechanism by which acetazolamide could oppose this blunting effect remains to be established.…”

Angiotensin-Converting Enzyme and Genetics at High Altitude

“…Exercise at HA still produces a rise in PRA and PAC (Maher et al, 1975, Milledge et al, 1983a, Lawrence et al, 1991, Rock et al, 1993, though not all studies confirm this (Zaccaria et al, 1998). The rise in PAC with exercise at HA is of smaller magnitude than at SL (Bouissou et al, 1989 andBartsch et al, 1991), and has been found to be more subdued with acute, rather than chronic (14-16 days), exposure (Rock et al, 1993).…”

Recovery of plasma volume after 1 week of exposure at 4,350 m

“…Two events occurring during RSL may initiate PV recovery through water retention: (1) high-altitude hypovolemia, which induced appropriate hormonal changes, and (2) acute reoxygenation, i.e., suppression of hypoxia, known to be a potent stimulator of atrial natriuretic factor (ANF) secretion and an inhibitor of aldosterone release [2,20]. The present study describes PV recovery upon early RSL after high-altitude exposure with concomitant changes in major fluid-regulating hormones and water intake/output.…”