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Experimental Biology and Medicine 226:847-853 (2001)
© 2001 Society for Experimental Biology and Medicine

ORIGINAL ARTICLE

Reduced Oxygen Tension Increases Atrial Natriuretic Peptide Release from Atrial Cardiocytes

James R. Klinger,1, Linda Pietras, Rod Warburton and Nicholas S. Hill

Division of Pulmonary, Sleep, and Critical Care Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island 02903

To test the hypothesis that reduced oxygen tension stimulates cardiac atrial natriuretic peptide (ANP) secretion, we measured ANP release and expression in neonatal rat atrial and ventricular cardiac myocytes exposed to 45 min and 3, 6, and 24 hr of 3% or 21% oxygen. In atrial cardiocytes, the percentage of increase in culture media ANP concentration from baseline was greater 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 increase in culture media ANP concentration was seen at 45 min (284% ± 27% vs. 201% ± 16%, P = NS) or 24 hr (2499% ± 250% vs. 2426% ± 195%). There was a significant increase in cellular ANP content between 3 and 24 hr in atrial 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 were not affected by oxygen tension. In ventricular cardiocytes, oxygen tension 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 may contribute to the elevation in plasma ANP seen during acute hypoxia.

Key Words: anoxia • atrial natriuretic factor • pulmonary hypertension • heart




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