Data/hora: 10/06/2024 09:16:24

Provedor de dados: | Brazilian Journal of Medical and Biological Research
País: | Brazil
Título: | Nitric oxide synthesis and biological functions of nitric oxide released from ruthenium compounds
Autores: | Pereira,A.C.; Paulo,M.; Araújo,A.V.; Rodrigues,G.J.; Bendhack,L.M.
Data: | 2011-09-01
Ano: | 2011
Palavras-chave: | Nitric oxide; Vasodilatation; Ruthenium complex; NO-synthase; Resistance artery; Conduit vessel.
Resumo: | During three decades, an enormous number of studies have demonstrated the critical role of nitric oxide (NO) as a second messenger engaged in the activation of many systems including vascular smooth muscle relaxation. The underlying cellular mechanisms involved in vasodilatation are essentially due to soluble guanylyl-cyclase (sGC) modulation in the cytoplasm of vascular smooth cells. sGC activation culminates in cyclic GMP (cGMP) production, which in turn leads to protein kinase G (PKG) activation. NO binds to the sGC heme moiety, thereby activating this enzyme. Activation of the NO-sGC-cGMP-PKG pathway entails Ca2+ signaling reduction and vasodilatation. Endothelium dysfunction leads to decreased production or bioavailability of endogenous NO that could contribute to vascular diseases. Nitrosyl ruthenium complexes have been studied as a new class of NO donors with potential therapeutic use in order to supply the NO deficiency. In this context, this article shall provide a brief review of the effects exerted by the NO that is enzymatically produced via endothelial NO-synthase (eNOS) activation and by the NO released from NO donor compounds in the vascular smooth muscle cells on both conduit and resistance arteries, as well as veins. In addition, the involvement of the nitrite molecule as an endogenous NO reservoir engaged in vasodilatation will be described.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000900017
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2011007500084
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.44 n.9 2011
Fonte: | info:eu-repo/semantics/openAccess