Angiotensin II induces proliferation of human cerebral artery smooth muscle cells through a basic fibroblast growth factor (bFGF) dependent mechanism.
Remodeling of cerebral arteries in hypertension produces thickened vessel walls associated with atherosclerotic plaque formation. In both thickening and plaque formation, proliferation of vascular smooth muscle cells is a hallmark. Genetically hypertensive rats treated with an angiotensin II (Ang II) AT1 receptor antagonist inhibited thickening of cerebral arteries suggesting a mitogenic action of Ang II on cerebral arterial VSMC (CVSMC). However, in studies using smooth muscle cells cultured from peripheral arteries, Ang II causes cell hypertrophy, but not proliferation. We determined the effect of Ang II on proliferation of cultured human CVSMC. CVSMC were cultured from the basilar artery obtained at autopsy. Ang II (10(-7) M) stimulated proliferation determined by counting cells and mitochondrial activity assay. Synthesis and release of basic fibroblast growth factor (bFGF) was essential for Ang II-stimulated proliferation. These findings are consistent with the notion that Ang II stimulates CVSMC proliferation thereby contributing to vessel remodeling.
Wang
Zhongbiao
Z
Division of Basic Medical Science, Mercer University School of Medicine and Medical Center of Central Georgia, 1550 College Street, Macon, GA 31207, USA. wang_z@mercer.edu
Rao
Pulipaka J
PJ
Shillcutt
Samuel D
SD
Newman
Walter H
WH
D000804:Angiotensin II / Q000378:metabolism* / Q000494:pharmacology; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002536:Cerebral Arteries / Q000187:drug effects* / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism
D016222:Fibroblast Growth Factor 2; D000804:Angiotensin II