Atrial natriuretic peptide exerts protective action against angiotensin II-induced cardiac remodeling by attenuating inflammation via endothelin-1/endothelin receptor A cascade View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-09

AUTHORS

Shuichi Fujita, Naoshi Shimojo, Fumio Terasaki, Kaoru Otsuka, Noriko Hosotani, Yuka Kohda, Takao Tanaka, Tomohiro Nishioka, Toshimichi Yoshida, Michiaki Hiroe, Yasushi Kitaura, Nobukazu Ishizaka, Kyoko Imanaka-Yoshida

ABSTRACT

We aimed to investigate whether atrial natriuretic peptide (ANP) attenuates angiotensin II (Ang II)-induced myocardial remodeling and to clarify the possible molecular mechanisms involved. Thirty-five 8-week-old male Wistar-Kyoto rats were divided into control, Ang II, Ang II + ANP, and ANP groups. The Ang II and Ang II + ANP rats received 1 μg/kg/min Ang II for 14 days. The Ang II + ANP and ANP rats also received 0.1 μg/kg/min ANP intravenously. The Ang II and Ang II + ANP rats showed comparable blood pressure. Left ventricular fractional shortening and ejection fraction were lower in the Ang II rats than in controls; these indices were higher (P < 0.001) in the Ang II + ANP rats than in the Ang II rats. In the Ang II rats, the peak velocity of mitral early inflow and its ratio to atrial contraction-related peak flow velocity were lower, and the deceleration time of mitral early inflow was significantly prolonged; these changes were decreased by ANP. Percent fibrosis was higher (P < 0.001) and average myocyte diameters greater (P < 0.01) in the Ang II rats than in controls. ANP decreased both myocardial fibrosis (P < 0.01) and myocyte hypertrophy (P < 0.01). Macrophage infiltration, expression of mRNA levels of collagen types I and III, monocyte chemotactic protein-1, and a profibrotic/proinflammatory molecule, tenascin-C (TN-C) were increased in the Ang II rats; ANP significantly decreased these changes. In vitro, Ang II increased expression of TN-C and endothelin-1 (ET-1) in cardiac fibroblasts, which were reduced by ANP. ET-1 upregulated TN-C expression via endothelin type A receptor. These results suggest that ANP may protect the heart from Ang II-induced remodeling by attenuating inflammation, at least partly through endothelin 1/endothelin receptor A cascade. More... »

PAGES

646-657

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00380-012-0311-0

DOI

http://dx.doi.org/10.1007/s00380-012-0311-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1011797843

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23277455


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