PROTECTIVE EFFECT OF ATRIAL-NATRIURETIC-PEPTIDE ON ELECTRICAL-FIELD-STIMULATED RAT VENTRICULAR STRIPS DURING HYPOXIA

We have previously shown that atrial natriuretic peptide reduces lacta te accumulation in non-beating rat ventricular myocardium exposed to h ypoxic conditions, and that hypoxia induces release of atrial natriure tic peptide from isolated rat atrial tissue. In these studies we sugge sted that atrial natriuretic peptide may be physiologically important for protection of the myocardium during periods of oxygen deficit. In the present study, we used isolated strips of rat right ventricle, con tracted by electrical-field-stimulation, as a model of a beating myoca rdium. After contraction stabilization, hypoxic conditions were introd uced through aeration with 20% O-2, held for 20 or 30 min., and then i nterrupted by reoxygenation with 95% O-2. The contractile force was re corded and the percentage regain of the contractions after reoxygenati on was considered as an indication of the amount of cell damage induce d during the period of hypoxia. The results show that after 30 min. of hypoxia and subsequent reoxygenation, ventricular strips treated with atrial natriuretic peptide (0.1 mu M) recovered 67.9+/-2.8% of the pr ehypoxic force of contraction; control strips from the same ventricle regained 44.9+/-4.4% (P=0.015) of their initial contractile activity. After 20 min. of hypoxia followed by reoxygenation, a ventricular stri p incubated together with an atrium regained 78.6+/-2.4% of the prehyp oxic force of contraction as compared to a 60.2+/-2.7% regain (P=0.002 ) for the control strip. We conclude that atrial natriuretic peptide p rotects the working ventricular myocardium during hypoxia, which furth er supports our previously reported suggestion that the effect on myoc ardial metabolism is physiologically relevant during situations of oxy gen deficit in heart muscle.