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 at rial natriuretic peptide from atrial tissue. Among these, stretching o f atrial myocytes is considered the most important. In a recent study we showed that atrial natriuretic peptide increased cGMP and reduced l actate accumulation during hypoxia in rat ventricular myocardium. This suggests that atrial natriuretic peptide has a beneficial metabolic e ffect during hypoxia and raises the question whether hypoxia alone ind uces release of atrial natriuretic peptide. The right atrium and piece s of the right ventricle, from rats, were incubated in polyethylene vi als containing 3 ml Krebs bicarbonate buffer equilibrated with 75% N-2 + 20% O-2 + 5% CO2 (= hypoxic conditions) or 95% O-2 + 5% CO2 (= norm oxic conditions). After 10 min, the ventricular tissues and aliquots o f the buffer were frozen. Cyclic GMP was analyzed in the ventricular t issue and atrial natriuretic peptide was analyzed in the buffer sample s. The results show that the release of atrial natriuretic peptide dur ing hypoxia significantly exceeds the release under normoxic condition s. The hypoxia-induced release of atrial natriuretic peptide over time is characterized by an s-shaped curve with the steepest slope after a bout 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 ventric ular myocardium when oxygen tension is low. Together with our earlier results, this finding suggests that atrial natriuretic peptide might h ave an important physiological function in protecting the myocardium d uring conditions of oxygen deficiency.