NT-proBNP does not rise on acute ascent to high altitude.

The response of brain natriuretic peptide (BNP) to acute ascent to altitude is of interest as a surrogate for ventricular function and because BNP is involved in the normal homeostasis of the pulmonary vasculature. The structurally related hormone atrial natriuretic pressure (ANP) has been demonstrated to be elevated at altitude and implicated in natriuresis. We measured plasma concentrations of ANP and NT-proBNP (a more stable BNP precursor) in 10 healthy non-HAPE-susceptible lowlanders during acute exposure to 5200 m on the Apex 2 expedition to Bolivia. Systolic pulmonary artery pressure (PASP) was measured using tricuspid regurgitant jet estimation by echocardiography. Despite a significant rise in the PASP, NT-proBNP did not rise. A small decrease in NT-pro BNP occurred after 7 days at high altitude. There was no significant change in ANP levels. The lack of any increase in NT-proBNP in healthy resting subjects supports the view that ventricular function is well preserved and suggests that BNP is not playing a significant role in altered pulmonary artery pressure.