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Angiotensin II receptor antagonist TCV-116 induces regression of hypertensive left ventricular hypertrophy in vivo and inhibits the intracellular signaling pathway of stretch-mediated cardiomyocyte hypertrophy in vitro.
Author(s) -
Motoki Kojima,
Ichiro Shiojima,
Tsutomu Yamazaki,
Issei Komuro,
Zhiyong Zou,
Y Wang,
Takuya Mizuno,
Ken Ueki,
Kazuyuki Tobe,
Takuya Kadowaki
Publication year - 1994
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.89.5.2204
Subject(s) - medicine , hydralazine , endocrinology , muscle hypertrophy , angiotensin ii , renin–angiotensin system , myocyte , left ventricular hypertrophy , receptor , blood pressure
Previous studies have demonstrated that angiotensin II (Ang II) acts as a growth-promoting factor directly on cardiac myocytes and that angiotensin-converting enzyme inhibitor induces regression of hypertrophied hearts both in experimental animals and in humans. These results suggest that the renin-angiotensin system (RAS) is involved in the formation of left ventricular hypertrophy (LVH). To elucidate the role of RAS in the progression of cardiac hypertrophy, we evaluated the effect of an Ang II receptor antagonist on LVH in spontaneously hypertensive rats (SHRs) and investigated the molecular mechanisms by which antagonizing Ang II receptors reduces cell hypertrophy of myocytes using the in vitro model of mechanical stretch.

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