Reduced oxygen tension increases atrial natriuretic peptide release from atrial cardiocytes

To test the hypothesis that reduced oxygen tension stimulates cardiac atria l natriuretic peptide (ANP) secretion, we measured ANP release and expressi on in neonatal rat atrial and ventricular cardiac myocytes exposed to 45 mi n and 3, 6, and 24 hr of 3% or 21% oxygen. In atrial cardiocytes, the perce ntage of increase in culture media ANP concentration from baseline was grea ter in cells exposed to 3% than in cells exposed to 21% oxygen after 3 hr ( 814% +/- 52% vs. 567% +/- 33%, P < 0.05) and 6 hr of exposure (1639% +/- 91 % vs. 1155% +/- 73%, P < 0.05). No differences in the percentage of increas e in culture media ANP concentration was seen at 45 min (284% +/- 27% vs. 2 01% +/- 16%, P = NS) or 24 hr (2499% +/- 250% vs. 2426% +/- 195%). There wa s a significant increase in cellular ANP content between 3 and 24 hr in atr ial cardiocytes exposed to 21% oxygen (105% +/- 40% vs. 296% +/- 60%, P < 0 .05), but not in atrial cardiocytes exposed to 3% oxygen (118% +/- 20% vs. 180% +/- 26%, P = NS). Steady-state ANP mRNA levels in atrial cardiocytes w ere not affected by oxygen tension. In ventricular cardiocytes, oxygen tens ion did not affect ANP secretion, cellular ANP content, or steady-state ANP mRNA levels. We conclude that reduced oxygen tension increases release of ANP from atrial, but not ventricular cardiocytes and that this mechanism ma y contribute to the elevation in plasma ANP seen during acute hypoxia.