Oxido Nitrico

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Bueno, basicamente para los que no entienden ingles este estudio dice que el oxido nitrico es antihipertrofico

Nitric oxide attenuates Endothelin-1-induced activation of ERK1/2, PKB and Pyk2 in vascular smooth muscle cells by a cGMP-dependent pathway.
Bouallegue A, Bou Daou G, Srivastava A.

Physiology, University of Montreal, MONTREAL, Canada.

Nitric oxide (NO), in addition to its vasodilator action, has also been shown to antagonize the mitogenic and hypertrophic responses of growth factors and vasoactive peptides such as endothelin-1 (ET-1) in vascular smooth muscle cells (VSMCs). However, the mechanism by which NO exerts its anti-mitogenic and anti-hypertrophic effect remains unknown. Therefore, the aim of this study was to determine if NO generation would modify ET-1-induced signaling pathways involved in cellular growth, proliferation and hypertrophy in A-10 VSMC. Treatment of A-10 VSMCs with S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitroprusside (SNP), two NO donors, attenuated the ET-1-enhanced phosphorylation of several key components of growth promoting and hypertrophic signaling pathways such as ERK1/2, PKB and Pyk2. On the other hand, the inhibition of the endogenous NO generation by using N-nitro-L- arginine methyl ester (L-NAME), a NO synthase inhibitor, increased the ET-1-induced phophosphorylation of these signaling components. Since, NO mediates its effect principally through a cyclic GMP/soluble guanylyl cyclase (sGC) pathway, we investigated the role of these molecules in NO action. 8-Br-cGMP, a non-metabolizable and cell permeable analogue of cGMP, exhibited a similar effect to that of SNAP and SNP. Furthermore, oxadiazole quinoxalin (ODQ), an inhibitor of sGC, reversed the inhibitory effect of NO on ET-1-induced responses. SNAP treatment also decreased the protein synthesis induced by ET-1. Taken together, these data demonstrate that NO, in a cGMP-dependent manner, attenuated ET-1-induced phosphorylation of ERK1/2, PKB and Pyk2 and also antagonized the hypertrophic effects of ET-1. It may be suggested that NO-induced generation of cGMP contributes to the inhibition of ET-1-induced mitogenic and hypertrophic responses in VSMCs. Key words: Cell signaling, protein synthesis, endothelin-1, NO.

PMID: 17644565 [PubMed - as supplied by publisher]

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