Abstract
A large number of experimental studies have suggested that hypoxia may be a potent stimulus for the myocardial synthesis and release of A-type natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) [1]. However, these studies have evaluated either the effect of hypoxia on ANP and/or BNP production in isolated cardiomyocytes [2,3], isolated perfused 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].
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