Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P159

SFEBES2009 Poster Presentations Diabetes and metabolism (59 abstracts)

Brain natriuretic peptide shows no response to acute hypobaric hypoxia in humans

David Woods 1, , Tim Hooper 2 , Adrian Mellor 2 , Pete Hodkinson 3 , Rob Wakeford 2 , Bob Peaston 4 , Steve Ball 5 & Nic Green 3


1Newcastle and Northumbria NHS Trust, University of Newcastle, Newcastle, UK; 2Defence Medical Services, London, UK; 3RAF Henlow, Centre for Aviation Medicine, Bedfordshire, UK; 4Freeman Hospital, Newcastle, UK; 5Royal Victoria Infirmary, Newcastle, UK.


Background: Effective acclimatization to high altitude involves a natriuresis and diuresis facilitated by a suppressed aldosterone. Acute mountain sickness (AMS) is common but poorly understood. A cardiac hormone, brain natriuretic peptide (BNP), is released primarily in response to cardiomyocyte stretch but animal models suggest BNP secretion is also stimulated by acute hypoxia. An increase in BNP causes a diuresis, natriuresis and a reduction in aldosterone. We hypothesized that acute hypobaric hypoxia would elevate BNP.

Method: Seven healthy subjects (28±2.4 years; 70.3±14.8 kg; 172±8 cm) gave informed consent. Blood samples were taken for assay of BNP at rest. Subjects then entered a hypobaric chamber where barometric pressure was reduced at a rate equivalent to 4000 feet ascent per minute up to an altitude equivalent to 17 500 feet. After 25 min at this altitude a standardised 1 min exercise step-test was performed and blood samples taken pre- and post-exercise (with simultaneous recordings of oxygen saturation and heart rate). Subjects breathed ambient air throughout. BNP was analysed using Biosite Triage BNP test kits at sea level after satisfactory quality control checks and had been passed.

Results: Mean (±S.D.) Sa02 was 98.1±0.69; 68.1±2.89 and 62.2±5.3 at sea level; pre-exercise and post-exercise at 17 500 feet. Mean HR (±S.D.) was 65.4±9.2; 81.1±7.1 and 134.1±15.3 at sea level; 17 500 feet pre-exercise and 17 500 feet post-exercise. BNP remained <5 pg/ml in 6 of 7 subjects and showed no significant rise in the seventh subject (BNP 18.1 pg/ml pre-exercise, 18.9 post-exercise).

Conclusion: Acute hypobaric hypoxia with exercise induced significant hypoxaemia and tachycardia in all subjects. No significant rise in BNP occurred. BNP may not therefore be implicated in the natriuresis and diuresis of high altitude adaptation. Alternatively, it may be that the relatively acute (<40 min) hypoxic exposure is an insufficient stimuli to BNP secretion. Further experimentation under prolonged hypoxic conditions is underway.

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