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Cardiovascular Research 1996 31(1):117-123; doi:10.1016/S0008-6363(95)00168-9
© 1996 by European Society of Cardiology
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Copyright © 1996, European Society of Cardiology

Cocaine-stimulated endothelin-1 release is decreased by angiotensin-converting enzyme inhibitors in cultured endothelial cells

Karen D. Hendricks-Muñoz*,a, Rene P. Gerretsa, Rosemary D. Higginsa, Jose L. Muñozb and Vaughan V. Cainesa

aNeonatal Program, Department of Pediatrics, New York University Medical Center, New York, NY 10016, USA
bDivision of Pediatric Infectious Diseases, Department of Pediatrics, New York Medical College, New York, NY 10016, USA

* Corresponding author. 560 First Avenue, Tisch Hospital, Room H553, New York, New York 10016, USA. Tel. (+1-212) 263-5811; Fax (+1-212) 263-8458.

Objective: The primary aim was to determine the action of pathophysiologically relevant cocaine concentrations (10–7–10–5 M) on endothelin-1 (ET-1) release from cultured endothelial cells under various cellular conditions. Further aims were to evaluate the effect of angiotensin-converting enzyme inhibitors on cocaine-treated endothelial cells, to assess their potential for inhibition of ET-1-stimulated release. Methods: Endothelin-1 release into the media was evaluated by radioimmunoassay under basal conditions and after 24 h treatment of endothelial cells with cocaine hydrochloride (HCl), or cocaine HCl and ACE inhibitors, captopril and lisinopril. The effect of serum and plasma under these conditions was also investigated. Results: Cocaine HCl stimulated ET-1 release in a dose response fashion that was independent of plasma or serum factors. Furthermore, cocaine-stimulated ET-1 release was inhibited by administration of angiotensin-converting enzyme inhibitors captopril and lisinopril. Conclusions: These findings suggest that cocaine can directly stimulate endothelial cells to release ET-1 and that the observed increase is independent of serum or plasma factors. Furthermore, cocaine-stimulated endothelin-1 release appears to be mediated at least in part by the angiotensin system. These observations provide a framework for understanding the cellular mechanisms involved in cocaine-induced vasoconstriction.

KEYWORDS Endothelin-1 (ET-1); Angiotensin-converting enzyme (ACE); Human umbilical vein endothelial cells (HUVEC's); Bovine pulmonary artery endothelial cells (BPAEC's); Lactate dehydrogenase (LDH); Sulfhydryl (SH)


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