Angiotensin-II down-regulates cardiac natriuretic peptide receptor-A mediated anti-hypertrophic signaling in experimental rat hearts

被引：0

作者：

Gopi, Venkatachalam ^{[1
]}

Parthasarathy, Arumugam ^{[1
]}

Umadevi, Subramanian ^{[1
]}

Vellaichamy, Elangovan ^{[1
]}

机构：

[1] Univ Madras, Dept Biochem, Madras 600025, Tamil Nadu, India

来源：

INDIAN JOURNAL OF EXPERIMENTAL BIOLOGY | 2013年 / 51卷 / 01期

关键词：

Angiotensin-II; Atrial natriuretic peptide; Guanylyl cyclase activity; Left ventricular hypertrophy; Natriuretic peptide receptor-A; LEFT-VENTRICULAR HYPERTROPHY; CONVERTING ENZYME-INHIBITOR; GENE-EXPRESSION; GUANYLATE-CYCLASE; ACE-INHIBITION; FIBROSIS; MICE; CARDIOMYOCYTE; SYSTEM; DYSFUNCTION;

D O I：

暂无

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Atrial natriuretic peptide (ANP) exerts and-hypertrophic effects in the heart via natriuretic peptide receptor-A (NPR-A). However, ANP mediated anti-hypertrophic activity is decreased in the cardiomyopathic conditions. In the present investigation the in vivo effects of angiotensin II (Ang II), a hypertrophic agonist have been studied on the ventricular expression level of NPR-A in Wistar rat hearts. NPR-A expression at the protein and mRNA levels were found to be markedly reduced by 5-fold respectively in Ang II infused rats heart as compared with sham rat hearts. Moreover, cGMP production in response to ANP was reduced by 77% in the isolated cardiac membrane preparation from the Ang II infused rat hearts. Losartan treatment reversed NPR-A expression and responsiveness to ANP. This study suggests that Ang II down regulates cardiac NPR-A activity by suppressing Npr1 gene transcription.

引用

页码：48 / 55

页数：8

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