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Cardiovascular Research 2000 45(3):777-782; doi:10.1016/S0008-6363(99)00265-5
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

ACE-inhibition promotes apoptosis after balloon injury of rat carotid arteries

Anne Mette Holma,*, Claus Bøgelund Andersenb, Stig Haunsøa and Peter Riis Hansena

aDepartment of Medicine B2142, The Rigshospital, DK-2100 Copenhagen, Denmark
bDepartment of Pathology, The Rigshospital, DK-2100 Copenhagen, Denmark

* Corresponding author. Tel.: +45-35-456-738; fax: +45-35-456-743 amholm{at}hotmail.com

Objective: Angiotensin II stimulates vascular smooth muscle cell (VSMC) growth, and is considered to be an important mediator of intimal thickening after vascular injury. Recent evidence has indicated that VSMC apoptosis plays a major role in the response to balloon injury, and we therefore examined the effect of angiotensin converting enzyme (ACE)-inhibition on VSMC apoptosis and vascular lesion formation in the rat model of balloon injury. Methods: Male Sprague–Dawley rats were subjected to carotid artery balloon injury and randomised to a standard diet or a diet supplemented with 1 mg/ml captopril in the drinking water. Animals were sacrificed 2 and 14 days after injury for assessment of apoptosis and proliferation by in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling (TUNEL) and proliferating cell nuclear antigen (PCNA) immunohistochemistry, respectively. At 14 days post injury, vessel cross-sections were subjected to microscopic morphometry and total cell numbers were determined. Results: At 2 days after balloon injury, captopril-treated animals displayed a significant increase in the percentage of TUNEL-positive VSMCs in the medial area (12±4% vs. 1±1%; P<0.05) as compared to controls. This increase in early apoptosis was associated with decreased intimal cellularity 14 days post injury (238±47 cells/cross-section vs. 449±75 cells/cross-section; P<0.05), and a reduction of neointimal formation (0.13±0.02 mm2 vs. 0.23±0.04 mm2; P<0.05). The fraction of PCNA-positive VSMCs per cross-section 2 or 14 days after injury was not significantly altered by captopril administration. Conclusion: Captopril inhibits neointimal formation in the rat model of arterial injury by mechanisms involving induction of VSMC apoptosis.

KEYWORDS ACE inhibitors; Angiotensin; Apoptosis; Arteries; Restenosis


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