Mechanical stress activates angiotensin II type 1 receptor without the involvement of angiotensin II View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-05-16

AUTHORS

Yunzeng Zou, Hiroshi Akazawa, Yingjie Qin, Masanori Sano, Hiroyuki Takano, Tohru Minamino, Noriko Makita, Koji Iwanaga, Weidong Zhu, Sumiyo Kudoh, Haruhiro Toko, Koichi Tamura, Minoru Kihara, Toshio Nagai, Akiyoshi Fukamizu, Satoshi Umemura, Taroh Iiri, Toshiro Fujita, Issei Komuro

ABSTRACT

The angiotensin II type 1 (AT1) receptor has a crucial role in load-induced cardiac hypertrophy. Here we show that the AT1 receptor can be activated by mechanical stress through an angiotensin-II-independent mechanism. Without the involvement of angiotensin II, mechanical stress not only activates extracellular-signal-regulated kinases and increases phosphoinositide production in vitro, but also induces cardiac hypertrophy in vivo. Mechanical stretch induces association of the AT1 receptor with Janus kinase 2, and translocation of G proteins into the cytosol. All of these events are inhibited by the AT1 receptor blocker candesartan. Thus, mechanical stress activates AT1 receptor independently of angiotensin II, and this activation can be inhibited by an inverse agonist of the AT1 receptor. More... »

PAGES

499-506

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncb1137

DOI

http://dx.doi.org/10.1038/ncb1137

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045528986

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15146194


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