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1 The Hypertension & Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC, USA
* To whom correspondence should be addressed. E-mail: atallant{at}wfubmc.edu.
Peptide hormones, such as angiotensin II and endothelin, contribute to cardiac remodeling after myocardial infarction by stimulating myocyte hypertrophy and myofibroblast proliferation. In contrast, angiotensin-(1-7) [Ang-(1-7)] infusion following myocardial infarction reduced myocyte size and attenuated ventricular dysfunction and remodeling. We measured the effect of Ang-(1-7) on protein and DNA synthesis in cultured neonatal rat myocytes, to assess the role of the heptapeptide in cell growth. Ang-(1-7) significantly attenuated either fetal bovine serum- or endothelin-1-stimulated 3H-leucine incorporation into myocytes, with no effect on 3H-thymidine incorporation. [D-Alanine7]-angiotensin-(1-7) [[D-Ala7]-Ang-(1-7)], the selective AT(1-7) receptor antagonist, blocked the Ang-(1-7)-mediated reduction in protein synthesis in cardiac myocytes while AT1 and AT2 angiotensin peptide receptors were ineffective. Serum-stimulated ERK1/ERK2 mitogen-activated protein kinase activity was significantly decreased by Ang-(1-7) in myocytes, a response which was also blocked by [D-Ala7]-Ang-(1-7). Both rat heart and cardiac myocytes express the mRNA for the mas receptor and a 59 kDa immunoreactive protein was identified in both extracts of rat heart and cultured myocytes by Western blot hybridization using an antibody to mas, an Ang-(1-7) receptor. Transfection of cultured myocytes with an antisense oligonucleotide to the mas receptor blocked the Ang-(1-7)-mediated inhibition of serum-stimulated MAP kinase activation, while a sense oligonucleotide was ineffective. These results suggest that Ang-(1-7) reduces the growth of cardiomyocytes through activation of the mas receptor. Since Ang-(1-7) is elevated following treatment with angiotensin-converting enzyme inhibitors or AT1 receptor blockers, Ang-(1-7) may contribute to their beneficial effects on cardiac dysfunction and ventricular remodeling following myocardial infarction.
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