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. 2011 May;61(3):217-20.
doi: 10.1007/s12576-011-0141-3. Epub 2011 Mar 24.

Brain natriuretic peptide and acute hypobaric hypoxia in humans

David Woods  1 , Tim Hooper, Adrian Mellor, Pete Hodkinson, Rob Wakeford, Bob Peaston, Steve Ball, Nic Green
Affiliations

Brain natriuretic peptide and acute hypobaric hypoxia in humans

David Woods et al. J Physiol Sci. 2011 May.

Abstract

In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion.

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Conflict of interest statement

None.

Figures

Fig. 1
Fig. 1
Oxygen saturation (mean ± SEM) at ground level, at a simulated altitude of 5,334 m and following brief exercise at 5,334 m
See this image and copyright information in PMC

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