Effects of cocaine on vascular endothelium relaxing properties and the related mechanism were investigated in vitro in rabbit aorta. Several vasorelaxing agents with different mechanisms, i.e. acetylcholine, substance P, calcium ionophore A23187, 2,5-di-tert-butylhydroquinone, or sodium nitroprusside, were employed. Cocaine effects on the vascular response to relaxing agents in cumulative (acetylcholine, substance P, or A23187) or single dose (2,5-di-tert-butyl-hydroquinone) were performed in endothelium-intact aortic rings precontracted with phenylephrine. Relaxing activity of cumulative doses of sodium nitroprusside was evaluated in endothelium-denuded aortic rings, in the presence of cocaine. Cocaine significantly reduced endothelium-dependent relaxations induced by acetylcholine, or substance P. By contrast A23187 endothelium-mediated relaxation as well as endothelium-independent relaxation by sodium nitroprusside were unaffected by cocaine. Furthermore, cocaine significantly increased endothelium-dependent relaxation response to 2,5-di-tert-butylhydroquinone, a sarcoplasmic Ca2+-ATPase pump inhibitor, in the aortic rings. These findings indicate that cocaine reduces nitric oxide release from vascular endothelium apparently through the inhibiting action of Ca2+-ATPase pump. © 2001 Elsevier Science Ireland Ltd. All rights reserved.

Cocaine toxic effect on endothelium-dependent vasorelaxation: An in vitro study on rabbit aorta / Togna, Giuseppina Ines; Graziani, Manuela; Pierluigi, Russo; Caprino, Luciano. - In: TOXICOLOGY LETTERS. - ISSN 0378-4274. - STAMPA. - 123:1(2001), pp. 43-50. [10.1016/s0378-4274(01)00379-4]

Cocaine toxic effect on endothelium-dependent vasorelaxation: An in vitro study on rabbit aorta

TOGNA, Giuseppina Ines;GRAZIANI, Manuela;CAPRINO, Luciano
2001

Abstract

Effects of cocaine on vascular endothelium relaxing properties and the related mechanism were investigated in vitro in rabbit aorta. Several vasorelaxing agents with different mechanisms, i.e. acetylcholine, substance P, calcium ionophore A23187, 2,5-di-tert-butylhydroquinone, or sodium nitroprusside, were employed. Cocaine effects on the vascular response to relaxing agents in cumulative (acetylcholine, substance P, or A23187) or single dose (2,5-di-tert-butyl-hydroquinone) were performed in endothelium-intact aortic rings precontracted with phenylephrine. Relaxing activity of cumulative doses of sodium nitroprusside was evaluated in endothelium-denuded aortic rings, in the presence of cocaine. Cocaine significantly reduced endothelium-dependent relaxations induced by acetylcholine, or substance P. By contrast A23187 endothelium-mediated relaxation as well as endothelium-independent relaxation by sodium nitroprusside were unaffected by cocaine. Furthermore, cocaine significantly increased endothelium-dependent relaxation response to 2,5-di-tert-butylhydroquinone, a sarcoplasmic Ca2+-ATPase pump inhibitor, in the aortic rings. These findings indicate that cocaine reduces nitric oxide release from vascular endothelium apparently through the inhibiting action of Ca2+-ATPase pump. © 2001 Elsevier Science Ireland Ltd. All rights reserved.
2001
cocaine; endothelium; nitric oxide; rabbit aorta
01 Pubblicazione su rivista::01a Articolo in rivista
Cocaine toxic effect on endothelium-dependent vasorelaxation: An in vitro study on rabbit aorta / Togna, Giuseppina Ines; Graziani, Manuela; Pierluigi, Russo; Caprino, Luciano. - In: TOXICOLOGY LETTERS. - ISSN 0378-4274. - STAMPA. - 123:1(2001), pp. 43-50. [10.1016/s0378-4274(01)00379-4]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/249117
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