Please use this identifier to cite or link to this item:
Title: Orally administered rapamycin does not modify rat aortic vascular tone
Authors: Soares Neto, Milton Macedo [UNIFESP]
Di Marco, Giovana Seno [UNIFESP]
Casarini, Dulce Elena [UNIFESP]
Lima, Valter Correia de [UNIFESP]
Campos, Alexandre Holthausen [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 1-Feb-2007
Publisher: Lippincott Williams & Wilkins
Citation: Journal Of Cardiovascular Pharmacology. Philadelphia: Lippincott Williams & Wilkins, v. 49, n. 2, p. 96-99, 2007.
Abstract: Rapamycin (RP; rapamune, sirolimus) is a potent inhibitor of vascular smooth muscle cell proliferation and migration. RP was demonstrated to reduce vascular neointimal formation in different animal models of vascular smooth muscle cell proliferation, and clinical use of RP-eluting stents promotes significant reductions in in-stent resterrosis rates. However, high costs still preclude the widespread use of these devices. Oral administration of RP associated to bare metal stent delivery has been advocated as an effective and considerably less expensive alternative for restenosis prevention. It is noteworthy that the presence of RP-eluting stents has been associated with reduced endothelial-dependent vasodilation and coronary spasm. In addition, RP has been demonstrated to prevent vasculo-genesis. This study evaluated the effects of R-P on endothelium-dependent vascular tone and demonstrated that in vitro incubation with high concentrations of RP did not modify either contraction or relaxation of aortic rings. Similar results were obtained after in vivo administration of the drug. These findings suggest that function of adult, non-proliferative rat endothelial cells involved in vascular tone control is not affected by orally administered RP.
ISSN: 0160-2446
Other Identifiers:
Appears in Collections:Artigo

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.