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A critical cytoprotective role of endogenous adrenomedullin in acute myocardial infarction.

Abstract
Exogenous administration or transfection of adrenomedullin (AM) affords protection against ischaemia-reperfusion injury. Here we have examined the role of endogenous AM in regulating the development of myocardial infarction. Wild type (WT) and AM(+/-) mice underwent 30 min regional myocardial ischaemia and 120 min reperfusion. In AM(+/-) hearts, tetrazolium-determined infarct size was greater than in WT controls (27.9 +/- 2.0 vs. 17.7 +/- 2.4%, P < 0.01) and mortality rate was increased (35% vs. 14%, P < 0.05). Treatment with exogenous recombinant AM (200 ng/kg) prior to coronary occlusion rescued the ischaemia-reperfusion intolerant phenotype of AM(+/-) mice and further limited infarct development in WT mice. Administration of recombinant AM was associated with augmented phosphorylation of Akt and eNOS in early reperfusion suggesting a role for AM in regulating this survival pathway. These studies provide the first evidence that expression of AM is a critical factor regulating myocardial tolerance to ischaemia-reperfusion injury.
AuthorsShabaz A Hamid, Gary F Baxter
JournalJournal of molecular and cellular cardiology (J Mol Cell Cardiol) Vol. 41 Issue 2 Pg. 360-3 (Aug 2006) ISSN: 0022-2828 [Print] England
PMID16842816 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Peptides
  • Recombinant Proteins
  • Adrenomedullin
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Nos3 protein, mouse
  • Oncogene Protein v-akt
Topics
  • Adrenomedullin
  • Animals
  • Female
  • Gene Expression Regulation (drug effects)
  • Male
  • Mice
  • Myocardial Infarction (metabolism, prevention & control)
  • Myocardial Reperfusion Injury (metabolism, prevention & control)
  • Nitric Oxide Synthase Type II (metabolism)
  • Nitric Oxide Synthase Type III
  • Oncogene Protein v-akt (metabolism)
  • Peptides (metabolism, pharmacology)
  • Recombinant Proteins (metabolism, pharmacology)
  • Signal Transduction (drug effects)

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