title: Molecular mechanisms of the exaggerated growth of vascular smooth muscle cells in hypertension.
abstract: The molecular mechanisms of the exaggerated growth of vascular smooth muscle cells (VSMC) in hypertension are reviewed based on our previous experimental data. Spontaneously hypertensive rats (SHR)-derived VSMC increasingly express angiotensinogen, cathepsin D and angiotensin-converting enzyme (ACE) mRNAs, compared to cells from normotensive Wistar-Kyoto (WKY) rats, indicating the presence of an Ang II generating system in a homogeneous culture of VSMC from SHR. The produced Ang II then induces TGF-beta. SHR-derived VSMC show the distinct expression and abnormal regulation by Ang II of TGF-beta receptors when compared with cells from WKY rats, which express TGF-beta type II receptor predominantly to induce PDGF A-chain stimulation of VSMC growth. These findings imply that the increased growth of VSMC in hypertension is a primary event independent of high blood pressure, and is associated with endogenous Ang II-related growth factors.
authors.affiliation: Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Fukuda
mesh_terms: D000818:Animals; D002455:Cell Division / Q000502:physiology; D002478:Cells, Cultured; D006973:Hypertension / Q000473:pathology*; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018125:Receptors, Transforming Growth Factor beta / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000502:physiology
chemical_list: D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta