Hypoxia induces release of atrial natriuretic peptide in rat atrial tissue: a role for this peptide during low oxygen stress.

A variety of different factors have been shown to induce release of atrial natriuretic peptide from atrial tissue. Among these, stretching of atrial myocytes is considered the most important. In a recent study we showed that atrial natriuretic peptide increased cGMP and reduced lactate accumulation during hypoxia in rat ventricular myocardium. This suggests that atrial natriuretic peptide has a beneficial metabolic effect during hypoxia and raises the question whether hypoxia alone induces release of atrial natriuretic peptide. The right atrium and pieces of the right ventricle, from rats, were incubated in polyethylene vials containing 3 ml Krebs bicarbonate buffer equilibrated with 75% N2 + 20% O2 + 5% CO2 (= hypoxic conditions) or 95% O2 + 5% CO2 (= normoxic conditions). After 10 min, the ventricular tissues and aliquots of the buffer were frozen. Cyclic GMP was analyzed in the ventricular tissue and atrial natriuretic peptide was analyzed in the buffer samples. The results show that the release of atrial natriuretic peptide during hypoxia significantly exceeds the release under normoxic conditions. The hypoxia-induced release of atrial natriuretic peptide over time is characterized by an s-shaped curve with the steepest slope after about 10 min. In the presence of atrial tissue the intracellular level of cGMP in ventricular myocardium increased from 0.3 +/- 0.1 to 2.6 +/- 0.9 pmol/g w wt (P = 0.033, n = 6). We conclude that ANP is released from atrial tissue and induces increased formation of cGMP in ventricular myocardium when oxygen tension is low.(ABSTRACT TRUNCATED AT 250 WORDS)