title: [Effects of angiotensin II receptor blockers, angiotensin converting enzyme inhibitors, 3-hydroxy-3-methyl glutaryl (HMG) CoA reductase inhibitors, amlodipine and epalrestat on cultured basilar artery smooth muscle cell proliferation].
abstract: Proliferation of vascular smooth muscle cells (VSMC) stimulated by oxidative stresses and reactive oxygen species (ROS) may play a pivotal role in the pathogenesis of atherosclerosis. Antiatherosclerotic effects of angiotensin II receptor blockers, angiotensin converting enzyme inhibitors, HMG CoA reductase inhibitors, calcium channel blocker and epalrestat were studied with an in vitro guinea-pig basilar artery smooth muscle cell (GBa-SM3) culture system over 3 days incubated with 0 to 10% of fetal bovine serum. Results demonstrated that simvastatin (0.1 mM), fluvastatin (0.3 mM), amlodipine (0.2 mM) and epalrestat (1 mM) elicited significant (p < 0.05 or 0.01) antiproliferative effects, whereas losartan (1 mM), valsartan (1 mM), enalapril (0.1 mM), captopril (1 mM), trandolapril (0.01 mM), pravastatin (0.7 mM) did not. In conclusion, the present in vitro VSMC culture system may serve as a comprehensive screening method for pleiotropic effects of commonly used therapeutic agents.
authors.affiliation: Department of Hospital Pharmacy, Nakano General Hospital, 4-59-16 Chuou, Nakano-ku, Tokyo 164-8607, Japan. nghph@nakanosogo.or.jp
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Ida
authors.forename: Masazumi
authors.initials: M
authors.lastname: Hiraga
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Oishi
authors.forename: Masaatsu K
authors.initials: MK
authors.lastname: Uchida
authors.forename: Hirotoshi
authors.initials: H
authors.lastname: Echizen
mesh_terms: D017311:Amlodipine / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000517:prevention & control; D001488:Basilar Artery; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects*; D002478:Cells, Cultured; D003864:Depression, Chemical; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology*; D000077340:Fluvastatin; D006168:Guinea Pigs; D006903:Hydroxymethylglutaryl CoA Reductases / Q000494:pharmacology*; D007211:Indoles / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species; D012236:Rhodanine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D019821:Simvastatin / Q000494:pharmacology*; D053778:Thiazolidines
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D005229:Fatty Acids, Monounsaturated; D007211:Indoles; D017382:Reactive Oxygen Species; D053778:Thiazolidines; D017311:Amlodipine; C038131:epalrestat; D000077340:Fluvastatin; D012236:Rhodanine; D019821:Simvastatin; D006903:Hydroxymethylglutaryl CoA Reductases