Articles in PresS. Am J Physiol Heart Circ Physiol (January 2, 2009). doi:10.1152/ajpheart.00684.2008
Atrial natriuretic peptide increases inflammation, infarct size and mortality after experimental coronary occlusion
Aiilyan K. Houng,1,2 Rachel A. McNamee,1 Attila Kerner,1 Pallavi Sharma,1 Almois Mohamad,1 Jonathan Tronolone,1 Guy L. Reed.1,2
1
Cardiovascular Center, Medical College of Georgia, Augusta, Georgia, and 2Department of Medicine, University of Tennessee Health Science Center, Memphis, TN
Running title: Effect of ANP on myocardial infarct size and mortality
Corresponding author: Guy L. Reed, Dept. of Medicine, D334 Coleman, 956 Court Ave, Memphis, TN 38162. Email:
[email protected]; Tel (901) 448-5752 Fax (901) 448-1666
Copyright © 2009 by the American Physiological Society.
2 Abstract Acute coronary artery occlusion triggers the release of atrial natriuretic peptide (ANP) from the heart. ANP affects vasodilation, natriuresis and inflammation, but the integrated biologic effects of ANP on myocardial infarction are unknown. To elucidate these effects, the left anterior coronary artery was ligated in anesthetized, ANP-deficient (ANP-/-) and congenic wild-type (ANP+/+) mice. The survival of ANP-/- mice was markedly better (56%) 30 days post-infarction than the survival of ANP+/+ mice (20%, p < 0.01). Surviving mice were comparable initially, but ANP-/- mice developed more cardiac hypertrophy (p < 0.001) and had lower contractility indices 30 days after infarction (p < 0.05). Analysis 24 hours after coronary occlusion showed that ANP-/- mice had smaller infarcts than ANP+/+ mice (62.6% ± 12.1 vs. 100.8% ± 3.8, p
