Nature Communications (Feb 2017)

Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling

  • Chun-Hua Liu,
  • Zheng Gong,
  • Zong-Lai Liang,
  • Zhi-Xin Liu,
  • Fan Yang,
  • Yu-Jing Sun,
  • Ming-Liang Ma,
  • Yi-Jing Wang,
  • Chao-Ran Ji,
  • Yu-Hong Wang,
  • Mei-Jie Wang,
  • Fu-Ai Cui,
  • Amy Lin,
  • Wen-Shuai Zheng,
  • Dong-Fang He,
  • Chang-xiu Qu,
  • Peng Xiao,
  • Chuan-Yong Liu,
  • Alex R. B. Thomsen,
  • Thomas Joseph Cahill,
  • Alem W. Kahsai,
  • Fan Yi,
  • Kun-Hong Xiao,
  • Tian Xue,
  • Zhuan Zhou,
  • Xiao Yu,
  • Jin-Peng Sun

DOI
https://doi.org/10.1038/ncomms14335
Journal volume & issue
Vol. 8, no. 1
pp. 1 – 17

Abstract

Read online

Angiotensin II type 1 receptor (AT1R)-mediated acute catecholamine release is modulated by β-arrestin. Here the authors show that β-arrestin-1 recruits the Ca2+channel TRPC3 and the PLCγ to the AT1R-β-arrestin complex, triggering G protein-independent calcium influx and catecholamine secretion.