Brain natriuretic peptide and acute hypobaric hypoxia in humans

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.

Severe acute mountain sickness, brain natriuretic peptide and NT‐proBNP in humans

“…We also reported that mean LL AMS scores (mean ± SEM) for those with a BNP response vs. no BNP response at 5150 m were significantly different: 3.3 ± 0.5 vs. 0.75 ± 0.5 (P = 0.034) on day 10 and 3.3 ± 0.4 vs. 0 ± 0 (P = 0.003) on day 11. Although humans exposed to acute normobaric hypoxia (12% O 2 ) have been reported to show a 9% rise in NT-pro BNP (the inactive peptide cleaved from proBNP to release the active hormone BNP) (Due-Andersen et al 2008), our own work (Woods et al 2011b) and that of others (Cargill et al 1996) under conditions of acute hypobaric hypoxia has not demonstrated a rise in BNP. Although humans exposed to acute normobaric hypoxia (12% O 2 ) have been reported to show a 9% rise in NT-pro BNP (the inactive peptide cleaved from proBNP to release the active hormone BNP) (Due-Andersen et al 2008), our own work (Woods et al 2011b) and that of others (Cargill et al 1996) under conditions of acute hypobaric hypoxia has not demonstrated a rise in BNP.…”

Renal Function and Fluid Homeostasis

“…Evidence for BNP release at high altitude, however, is contradictory. In a hypobaric chamber study of several hours that caused oxygen saturations as low as 60 % this degree of hypoxemia did not increase BNP secretion [ 111 ]. Two studies of climbers ascending higher than 5050 m showed variable increases of up to fourfold over normal, but no relation to urinary sodium, urine volume or arterial saturation.…”

Markers of physiological stress during exercise under conditions of normoxia, normobaric hypoxia, hypobaric hypoxia, and genuine high altitude

“…The lack of a rise under conditions of HH warrants further comment. We have previously examined the BNP response to acute HH on two occasions: first, at a simulated altitude of 5334 m for 40 min involving a brief 1-min step-test (Woods et al 2011b) and, second, at a simulated 4800 m over 3 h with a brief 5-min step-test (Boos et al 2013). On neither occasion did we find a significant rise in BNP despite significant rises in PASP which we consider to be due to the brevity of the exercise stimulus.…”

“…Whether NH and HH are interchangeable means of simulating HA is not clearly understood, and yet, the literature is populated by studies examining the response to NH and HH with little consideration for whether there is any differential effect (Lundby et al 2005; Woods et al 2011b; Wille et al 2012; Li et al 2016). However, as illness at HA is relatively common and the pathophysiology of acute mountain sickness poorly understood (Schmerbach and Patzak 2013), there remains a need for both field and simulation studies.…”