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-β. SHR-derived VSMC show the distinct expression and abnormal regulation by Ang II of TGF-βreceptors when compared with cells from WKY rats, which express TGF-β 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.
