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Ethanol abrogates Angiotensin II-stimulated vascular smooth muscle cell growth.

Monique L. Cain, Robert L. Hester, Ernest B. Izevbigie

Med Sci Monit 2006; 12(5): BR162-168

ID: 450281

Published: 2006-05-01


Background: Aberrant vascular smooth muscle cell (VSMC) proliferation isone of the etiological factors for hypertension and stroke. Angiotensin II (Ang II) and ethanol (EtOH)have been shown to modulate the proliferation of vascular smooth muscle cells (VSMCs) individually, butthe combined effects of Ang II and EtOH on VSMC proliferative activities are unknown. The objective ofthis study was to determine the effects of EtOH, Ang II, and the combination of Ang II and EtOH on DNAsynthesis, cell number, cyclic AMP (cAMP) production, and Mitogen-Activated Protein Kinase (MAPK) or(p44/42) activities in murine primary VSMCs. Material/Methods: Cell growth was determined by [[sup]3[/sup]H] thymidineincorporation and confirmed by cell counts using a hemacytometer. Cyclic AMP assays were carried outusing commercially available kits. MAPK activity was determined by immunoprecipitation studies usingan ELK-1 fusion protein as a substrate. Results: Ang II (10 microM) stimulated DNA synthesis by four-fold(P

Keywords: Animals, Muscle, Smooth, Vascular - metabolism, Mitogen-Activated Protein Kinase 3 - metabolism, Mitogen-Activated Protein Kinase 1 - metabolism, MAP Kinase Signaling System - drug effects, Ethanol - pharmacology, Enzyme Activation - drug effects, Drug Interactions, DNA - biosynthesis, Cyclic AMP - biosynthesis, Cells, Cultured, Cell Proliferation - drug effects, Angiotensin II - pharmacology, Rats



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