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Articles in PresS, published online ahead of print January 11, 2002
J Appl Physiol, 10.1152/jap.00936.2001
Submitted on September 11, 2001
Accepted on December 10, 2001
1 Department of Clinical Physiology, Herlev Hospital, University of Copenhagen, Herlev, Denmark; Department of Anesthesia and Intensive Care, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
2 Department of Neuroanesthesia, Copenhagen University Hospital, Copenhagen, Denmark
3 Department of Anesthesia and Intensive Care, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
4 Copenhagen Muscle Research Centre, Copenhagen University Hospital, Copenhagen, Denmark
5 Department of Clinical Chemistry, Herlev Hospital, University of Copenhagen, Herlev, Denmark
6 Department of Medical Biology, University of Southern Denmark, Odense, Denmark
* To whom correspondence should be addressed. E-mail: mbestle{at}dadlnet.dk.
The effects of hypobaric hypoxemia on endocrine and renal parameters of body fluid homeostasis were investigated in eight normal males during a sojourn of eight days at an altitude of 4,559 m. The endocrine and renal responses to an osmotic stimulus (hypertonic saline, 5%, 3.6 ml x kg-1 over 1 hour) 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/kg), 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) as well as plasma vasopressin (1.14±0.16 to 0.38±0.06 pg/ml), 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) while urodilatin excretion rate decreased from day 2 (all changes: P<0.05 compared with sea level). The plasma AVP response and the antidiuretic response to hypertonic saline loading were unchanged, but the natriuretic response was attenuated. In conclusion, chronic hypobaric hypoxemia i) elevates the set point of the plasma osmolality to plasma vasopressin relationship, possibly due to the concurrent hypertension, thereby causing hypovolemia and hyperosmolality and ii) blunts the natriuretic response to hypertonic volume expansion possibly due to elevated circulating levels of norepinephrine and endothelin, reduced urodilatin synthesis, or attenuated inhibition of the renin-system.
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