PMID: 8964184Feb 1, 1996Paper

Angiotensin II mediates mechanical stress-induced cardiac hypertrophy

Diabetes Research and Clinical Practice
T YamazakiY Yazaki

Abstract

In order to elucidate the signal transduction pathway from external mechanical stress to nuclear gene expression in mechanical stress-induced cardiac hypertrophy, we examined the time course of activation of Raf-1 kinase (Raf-1), mitogen-activated protein kinase kinase (MAPKK) and MAP kinases (MAPKs) in neonatal rat cardiac myocytes. Mechanical stretch transiently activated Raf-1 and MAPKK with a peak at 2 and 5 min after stretch, respectively. In addition, MAPKs were maximally activated at 8 min after stretch. Next, the relationship between stretch-induced hypertrophy and the cardiac reninangiotensin system was investigated. When the stretch-conditioned culture medium was transferred to non-stretched cardiac myocytes, the medium activated MAPK activity slightly but significantly, and the activation was completely blocked by the type I angiotensin II (AngII) receptor antagonist, CV-11974. Moreover, in in vivo studies using spontaneously hypertensive rats, hypertension-induced cardiac hypertrophy was significantly reduced by treatment with subpressure doses of CV-11974. In addition, CV-11974 reduced the isozymic transition of MHC from VI to V3 and inhibited the accumulation of collagen fibers in the extracellular space of the my...Continue Reading

References

Jul 30, 1992·Nature·J M KyriakisJ Avruch
Jan 1, 1989·Clinical and Experimental Hypertension. Part A, Theory and Practice·W LinzD Ganten
Jan 1, 1993·Annual Review of Physiology·I Komuro, Y Yazaki

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Citations

Jun 13, 2015·Journal of Diabetes Research·Erin E GordonAndrew W Norris
Mar 7, 2001·In Vitro Cellular & Developmental Biology. Animal·C E MillerP R Chess
May 26, 2006·American Journal of Physiology. Cell Physiology·Michael D Godeny, Peter P Sayeski
Jan 27, 2010·Journal of Cardiovascular Pharmacology and Therapeutics·Weihua ZhangNaranjan S Dhalla
Mar 6, 2009·Hypertension Research : Official Journal of the Japanese Society of Hypertension·Jun IwanamiMasatsugu Horiuchi

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