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Ruthenium Complex Improves the Endothelial Function in Aortic Rings From Hypertensive Rats

BACKGROUND: The endothelium is a monolayer of cells that extends on the vascular inner surface, responsible for the modulation of vascular tone. By means of the release of nitric oxide (NO), the endothelium has an important protective function against cardiovascular diseases. OBJECTIVE: Verify if ci...

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Detalles Bibliográficos
Autores principales: Vatanabe, Izabela Pereira, Rodrigues, Carla Nascimento dos Santos, Buzinari, Tereza Cristina, de Moraes, Thiago Francisco, da Silva, Roberto Santana, Rodrigues, Gerson Jhonatan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira de Cardiologia - SBC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576116/
https://www.ncbi.nlm.nih.gov/pubmed/28678930
http://dx.doi.org/10.5935/abc.20170090
Descripción
Sumario:BACKGROUND: The endothelium is a monolayer of cells that extends on the vascular inner surface, responsible for the modulation of vascular tone. By means of the release of nitric oxide (NO), the endothelium has an important protective function against cardiovascular diseases. OBJECTIVE: Verify if cis- [Ru(bpy)(2)(NO(2))(NO)](PF(6))(2) (BPY) improves endothelial function and the sensibility of conductance (aorta) and resistance (coronary) to vascular relaxation induced by BPY. METHODS: Normotensive (2K) and hypertensive (2K-1C) Wistar rats were used. For vascular reactivity study, thoracic aortas were isolated, rings with intact endothelium were incubated with: BPY(0.01 to10 µM) and concentration effect curves to acetylcholine were performed. In addition, cumulative concentration curves were performed to BPY (1.0 nM to 0.1 µM) in aortic and coronary rings, with intact and denuded endothelium. RESULTS: In aorta from 2K-1C animals, the treatment with BPY 0.1µM increased the potency of acetylcholine-induced relaxation and it was able to revert the endothelial dysfunction. The presence of the endothelium did not modify the effect of BPY in inducing the relaxation in aortas from 2K and 2K-1C rats. In coronary, the endothelium potentiated the vasodilator effect of BPY in vessels from 2K and 2K-1C rats. CONCLUSION: Our results suggest that 0.1 µM of BPY is able to normalize the relaxation endothelium dependent in hypertensive rats, and the compound BPY induces relaxation in aortic from normotensive and hypertensive rats with the same potency. The endothelium potentiate the relaxation effect induced by BPY in coronary from normotensive and hypertensive rats, with lower effect on coronary from hypertensive rats.