Does hypoxemia have an impact on the cardiac release and circulating concentrations of natriuretic peptides in humans in vivo?

A large number of experimental studies have suggested that hypoxia may be a potent stimulus for the myocardial synthesis and release of Atype natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) [1]. However, these studieshaveevaluatedeither theeffectofhypoxiaonANP and/orBNPproduction in isolated cardiomyocytes [2,3], isolatedperfused hearts [4,5], or animals [5,6], or on the circulating concentrations of ANP, BNP, and/or N-terminal pro-BNP (NT-proBNP) but not on the cardiac release of these peptides in humans [7–9]. Accordingly, we performed two complementary studies to assess the relationship between the partial pressure of arterial oxygen (PaO2) and i) the cardiac release and ii) the circulating concentrations of natriuretic peptides in humans. First, we measured PaO2 and the transcardiac gradients of BNP and NT-proBNP (i.e., the differences between concentrations in the coronary sinus [BNPCS, NT-proBNPCS] and arterial plasma [BNPA, NT-proBNPA]) in patients undergoing a detailed non-invasive and invasive hemodynamic International Journal of Cardiology 167 (2013) 1046–1087