The effect of losartan on angiotensin II-induced cell proliferation in a rat aorta smooth muscle cell line
AUTOR(ES)
Tambelline, Natália, Oliveira, Karen, Olchanheski Junior, Luiz Renato, Sordi, Regina, Otuki, Michel Fleith, Favero, Giovani Marino, Fernandes, Daniel
FONTE
Brazilian Archives of Biology and Technology
DATA DE PUBLICAÇÃO
2012-04
RESUMO
The success of revascularization procedures is limited by recurrent stenosis, which is a narrowing of a blood vessels that results from neo-intimal hyperplasia. The renin-angiotensin-aldosterone system has been implicated in the pathogenesis of neo-intimal hyperplasia, and a role for angiotensin II in vascular smooth muscle cell proliferation has been proposed. There are at least two high-affinity subtypes of angiotensin II receptors, AT1 and AT2, both of which are seven-transmembrane G protein-coupled receptors. We investigated the effect of losartan, an AT1 receptor antagonist, on vascular smooth muscle cell proliferation using the A7r5 smooth cell line derived from rat aorta. Losartan was shown to prevent angiotensin II-induced cell proliferation, thereby suggesting that the effect of angiotensin II was mediated via AT1 receptors. These data strengthen the concept that inhibitors of the renin-angiotensin system can effectively prevent recurrent stenosis.
Documentos Relacionados
- Nitric oxide inhibits angiotensin II-induced migration of rat aortic smooth muscle cell. Role of cyclic-nucleotides and angiotensin1 receptors.
- Angiotensin II-induced stimulation of voltage-dependent Ca2+ currents in an adrenal cortical cell line.
- Muscle-specific expression of IGF-1 blocks angiotensin II–induced skeletal muscle wasting
- Natriuretic peptides inhibit angiotensin II-induced proliferation of rat cardiac fibroblasts by blocking endothelin-1 gene expression.
- Influence of angiotensin II-induced alterations in renal flow on excretion of cefonicid in isolated perfused rat kidneys.