Angiotensin II-induced ventricular hypertrophy and extracellular signal-regulated kinase activation are suppressed in mice overexpressing brain natriuretic peptide in circulation.

@article{Takahashi2003AngiotensinIV,
  title={Angiotensin II-induced ventricular hypertrophy and extracellular signal-regulated kinase activation are suppressed in mice overexpressing brain natriuretic peptide in circulation.},
  author={Nobuki Takahashi and Yoshihiko Saito and Koichiro Kuwahara and Masaki Harada and Ichiro Kishimoto and Yoshihiro Ogawa and Rika Kawakami and Yasuaki Nakagawa and Michio Nakanishi and Kazuwa Nakao},
  journal={Hypertension research : official journal of the Japanese Society of Hypertension},
  year={2003},
  volume={26 10},
  pages={847-53}
}
Atrial and brain (B-type) natriuretic peptides (ANP and BNP, respectively) are known to exert various cardioprotective effects. For instance, knocking out the expression of ANP, BNP, or their receptor, guanylyl cyclase-A, induces cardiac hypertrophy and/or fibrosis. The cardiac effects of elevated circulating natriuretic peptides are less well understood, however. We therefore compared angiotensin (Ang) II-induced cardiac hypertrophy and fibrosis in BNP-transgenic (Tg) mice, in which… CONTINUE READING