Inhibition of TRPC6 channel activity contributes to the antihypertrophic effects of natriuretic peptides-guanylyl cyclase-A signaling in the heart.

@article{Kinoshita2010InhibitionOT,
  title={Inhibition of TRPC6 channel activity contributes to the antihypertrophic effects of natriuretic peptides-guanylyl cyclase-A signaling in the heart.},
  author={Hideyuki Kinoshita and Koichiro Kuwahara and Motohiro Nishida and Zhong Jian and Xianglu Rong and Shigeki Kiyonaka and Y. Matsumoto Kuwabara and Hitoshi Kurose and Ryuji Inoue and Yasuo Mori and Yuhao Li and Yasuaki Nakagawa and Satoru Usami and Masataka Fujiwara and Yuko Yamada and Takeya Minami and Kenji Ueshima and Kazuwa Nakao},
  journal={Circulation research},
  year={2010},
  volume={106 12},
  pages={1849-60}
}
RATIONALE Atrial and brain natriuretic peptides (ANP and BNP, respectively) exert antihypertrophic effects in the heart via their common receptor, guanylyl cyclase (GC)-A, which catalyzes the synthesis of cGMP, leading to activation of protein kinase (PK)G. Still, much of the network of molecular mediators via which ANP/BNP-GC-A signaling inhibit cardiac hypertrophy remains to be characterized. OBJECTIVE We investigated the effect of ANP-GC-A signaling on transient receptor potential… CONTINUE READING
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