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J Appl Physiol 92: 1911-1922, 2002. First published January 11, 2002; doi:10.1152/japplphysiol.00936.2001
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Vol. 92, Issue 5, 1911-1922, May 2002

Prolonged hypobaric hypoxemia attenuates vasopressin secretion and renal response to osmostimulation in men

Morten H. Bestle1,2, Niels V. Olsen3, Troels D. Poulsen2, Robert Roach4, Niels Fogh-Andersen5, and Peter Bie6

1 Departments of Clinical Physiology and 5 Clinical Chemistry, Herlev Hospital, University of Copenhagen, DK-2730 Herlev; 2 Department of Anesthesia and Intensive Care, Gentofte Hospital, University of Copenhagen, DK-2900 Hellerup; 3 Department of Neuroanesthesia, and 4 Copenhagen Muscle Research Centre, Copenhagen University Hospital, DK-2100 Copenhagen; and 6 Department of Medical Biology, University of Southern Denmark, Odense, DK-5000 Odense, Denmark

Effects of hypobaric hypoxemia on endocrine and renal parameters of body fluid homeostasis were investigated in eight normal men during a sojourn of 8 days at an altitude of 4,559 m. Endocrine and renal responses to an osmotic stimulus (5% hypertonic saline, 3.6 ml/kg over 1 h) were investigated at sea level and on day 6 at altitude. Several days of hypobaric hypoxemia reduced body weight (-2.1 ± 0.4 kg), increased plasma osmolality (+5.3 ± 1.4 mosmol/kgH2O), elevated blood pressure (+12 ± 1 mmHg), reduced creatinine clearance (122 ± 6 to 96 ± 10 ml/min), inhibited the renin system (19.5 ± 2.0 to 10.9 ± 0.9 mU/l) and plasma vasopressin (1.14 ± 0.16 to 0.38 ± 0.06 pg/ml), and doubled circulating levels of norepinephrine (103 ± 16 to 191 ± 35 pg/ml) and endothelin-1 (3.0 ± 0.2 to 6.3 ± 0.6 pg/ml), whereas urodilatin excretion rate decreased from day 2 (all changes P < 0.05 compared with sea level). Plasma arginine vasopressin response and the antidiuretic response to hypertonic saline loading were unchanged, but the natriuretic response was attenuated. In conclusion, chronic hypobaric hypoxemia 1) elevates the set point of plasma osmolality-to-plasma vasopressin relationship, possibly because of concurrent hypertension, thereby causing hypovolemia and hyperosmolality, and 2) blunts the natriuretic response to hypertonic volume expansion, possibly because of elevated circulating levels of norepinephrine and endothelin, reduced urodilatin synthesis, or attenuated inhibition of the renin system.

endothelin-1; hypertonic saline; sodium excretion; urodilatin


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