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Endothelial Actions of ANP Enhance Myocardial Inflammatory Infiltration in the Early Phase After Acute Infarction
Author(s) -
Wen Chen,
Annett Spitzl,
Denise Mathes,
Viacheslav O. Nikolaev,
Franziska Werner,
Johannes Weirather,
Katarina Špiranec,
Katharina Röck,
Jens W. Fischer,
Ulrike Kämmerer,
David Stegner,
Hideo A. Baba,
Ulrich Hofmann,
Stefan Frantz,
Michaela Kühn
Publication year - 2016
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.115.307196
Subject(s) - tumor necrosis factor alpha , inflammation , knockout mouse , endothelial dysfunction , phosphodiesterase , medicine , necrosis , endothelial activation , endocrinology , hypoxia (environmental) , microcirculation , cancer research , immunology , biology , receptor , chemistry , biochemistry , enzyme , organic chemistry , oxygen
In patients after acute myocardial infarction (AMI), the initial extent of necrosis and inflammation determine clinical outcome. One early event in AMI is the increased cardiac expression of atrial natriuretic peptide (NP) and B-type NP, with their plasma levels correlating with severity of ischemia. It was shown that NPs, via their cGMP-forming guanylyl cyclase-A (GC-A) receptor and cGMP-dependent kinase I (cGKI), strengthen systemic endothelial barrier properties in acute inflammation.

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