Document Detail


Atrial natriuretic peptide increases inflammation, infarct size, and mortality after experimental coronary occlusion.
MedLine Citation:
PMID:  19122164     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute coronary artery occlusion triggers the release of atrial natriuretic peptide (ANP) from the heart. ANP affects vasodilation, natriuresis, and inflammation, but the integrated biological 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%) at 30 days postinfarction 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 indexes 30 days after infarction (P < 0.05). An analysis 24 h after coronary occlusion showed that ANP(-/-) mice had smaller infarcts than ANP(+/+) mice (62.6 +/- 12.1 vs. 100.8 +/- 3.8%, P < 0.001) adjusted for comparable areas at risk for ischemia. The administration of ANP to ANP(-/-) mice via osmotic minipumps significantly enlarged infarct size to levels comparable with those observed in ANP(+/+) mice (P < 0.05). There was no difference in neutrophil migration into the noninfarcted myocardium of ANP(-/-) mice undergoing actual versus sham-operated coronary occlusion. By comparison, after coronary occlusion, the neutrophil infiltration into the myocardium was enhanced in ANP(+/+) (P < 0.0005) and ANP(-/-) mice administered ANP (P < 0.0005). The expression of P-selectin, a molecule that mediates neutrophil adhesion, was significantly greater after coronary occlusion in the vasculature of ANP(+/+) or ANP(-/-) mice treated with ANP than in ANP(-/-) mice (P < 0.002). Taken together, these results indicate that ANP increases P-selectin, neutrophil infiltration, infarct size, and mortality following experimental coronary occlusion.
Authors:
Aiilyan K Houng; Rachel A McNamee; Attila Kerner; Pallavi Sharma; Almois Mohamad; Jonathan Tronolone; Guy L Reed
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-01-02
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  296     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-03-03     Completed Date:  2009-04-09     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H655-61     Citation Subset:  IM    
Affiliation:
Cardiovascular Center, Medical College of Georgia, Augusta, Georgia, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Atrial Natriuretic Factor / administration & dosage,  deficiency,  genetics,  metabolism*
Cardiomegaly / etiology,  metabolism
Coronary Occlusion / complications*,  metabolism,  pathology,  physiopathology
Disease Models, Animal
Hemodynamics
Inflammation / etiology*,  metabolism,  pathology,  physiopathology
Infusion Pumps, Implantable
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction
Myocardial Infarction / etiology*,  metabolism,  pathology,  physiopathology
Myocardium / metabolism*,  pathology
Neutrophil Infiltration
P-Selectin / metabolism
Time Factors
Grant Support
ID/Acronym/Agency:
HL-508496/HL/NHLBI NIH HHS; HL-78562/HL/NHLBI NIH HHS; R01 HL058496/HL/NHLBI NIH HHS; R01 HL078562/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/P-Selectin; 85637-73-6/Atrial Natriuretic Factor
Comments/Corrections

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