FEBS Letters · 1993 · 86 citations · 23 references
Life SciencesCardiologyPhysiologyAnimal PhysiologyInflammationSignal TransductionCardiovascular MedicineCardiovascular Molecular PhysiologyCardiovascular PhysiologyVascular Injury RepairVascular PathologyVascular TraumaChymase BiologyIatrogenic Vascular InjuryVascular HealingVascular Smooth Muscle DysfunctionVascular Smooth Muscle Regulation
Participation of angiotensin II in the myointimal proliferation following a vascular injury was postulated. This study assessed the potential involvement of the local angiotensin II-forming enzymes in injured arteries of dogs. The potential angiotensin II-forming enzymes are angiotensin-converting enzyme (ACE) and chymostatin-sensitive angiotensin II-generating enzyme (CAGE) which is highly homologous to or could be identical to the mast cell chymase. Both ACE and CAGE catalyze the conversion of angiotensin I to angiotensin II. We found that the enzymatic activities of ACE and CAGE, and the mRNA levels of ACE and chymase were increased in the injury-induced hypertrophied vessels. The results suggest that ACE and CAGE participate in the hypertrophy through the production of angiotensin II which is a growth promoter for vascular smooth muscle cells.
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Inhibitors of Angiotensin-Converting Enzyme Prevent Myointimal Proliferation After Vascular Injury
Jerry S. Powell, Jean-Paul Clozel, Rita Müller et al. · Science · 1989 · 1.1K citations
Medicine, Cardiology, Pharmacology +10
Circulation · 1992 · 544 citations · Full text
Medicine, Cardiology, Pharmacology +17