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(Received for publication, December 31, 1996, and in revised form, March 25, 1997)
From the Department of Internal Medicine (1st Division), Kobe
University School of Medicine, Kobe 650, Japan and the
§ Molecular Cardiology Unit, Research Institute of
Angiocardiology and Cardiovascular Clinic, Kyushu University School of
Medicine, Fukuoka 812-82, Japan
Angiotensin II (ANG II), a potent hypertrophic
factor of vascular smooth muscle cells (VSMC), induces activation of
the ras protooncogene product (Ras) and mitogen-activated
protein (MAP) kinases and subsequent stimulation of protein synthesis
in VSMC. In the present study, we examined whether Ras activation is
required for ANG II-induced MAP kinase activation and stimulation of
protein synthesis in cultured rat VSMC. Pretreatment with tyrosine
kinase inhibitors, genistein and herbimycin A, or a putative
phosphatidylinositol 3-kinase inhibitor, wortmannin, completely blocked
ANG II-induced Ras activation, whereas neither of them had an effect on
ANG II-induced MAP kinase activation. Adenovirus-mediated expression of
a dominant negative mutant of Ha-Ras completely inhibited ANG
II-induced Ras activation but failed to inhibit MAP kinase activation
and stimulation of protein synthesis by this vasoconstrictor. These results indicate that ANG II stimulates MAP kinases and protein synthesis by a Ras-independent pathway in VSMC.
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