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Recent advances in angiotensin II signaling BJMBR
Touyz,R.M.; Berry,C..
Angiotensin II (Ang II)* is a multifunctional hormone that influences the function of cardiovascular cells through a complex series of intracellular signaling events initiated by the interaction of Ang II with AT1 and AT2 receptors. AT1 receptor activation leads to cell growth, vascular contraction, inflammatory responses and salt and water retention, whereas AT2 receptors induce apoptosis, vasodilation and natriuresis. These effects are mediated via complex, interacting signaling pathways involving stimulation of PLC and Ca2+ mobilization; activation of PLD, PLA2, PKC, MAP kinases and NAD(P)H oxidase, and stimulation of gene transcription. In addition, Ang II activates many intracellular tyrosine kinases that play a role in growth signaling and...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Angiotensin receptors; Second messengers; Phospholipase; Protein kinase; Reactive oxygen species.
Ano: 2002 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2002000900001
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Reactive oxygen species and angiotensin II signaling in vascular cells: implications in cardiovascular disease BJMBR
Touyz,R.M..
Diseases such as hypertension, atherosclerosis, hyperlipidemia, and diabetes are associated with vascular functional and structural changes including endothelial dysfunction, altered contractility and vascular remodeling. Cellular events underlying these processes involve changes in vascular smooth muscle cell (VSMC) growth, apoptosis/anoikis, cell migration, inflammation, and fibrosis. Many factors influence cellular changes, of which angiotensin II (Ang II) appears to be amongst the most important. The physiological and pathophysiological actions of Ang II are mediated primarily via the Ang II type 1 receptor. Growing evidence indicates that Ang II induces its pleiotropic vascular effects through NADPH-driven generation of reactive oxygen species (ROS)....
Tipo: Info:eu-repo/semantics/article Palavras-chave: Vascular smooth muscle cells; Remodeling; Inflammation; Signal transduction; Reactive oxygen species.
Ano: 2004 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004000800018
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