Hypertension. 2006;48:797-803
Published online before print October 2, 2006, doi: 10.1161/01.HYP.0000242907.70697.5d
Published online before print October 2, 2006, doi: 10.1161/01.HYP.0000242907.70697.5d
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(Hypertension. 2006;48:797.)
© 2006 American Heart Association, Inc.
Brief Reviews |
Caveolin-Dependent Angiotensin II Type 1 Receptor Signaling in Vascular Smooth Muscle
From the Division of Cardiology (M.U.-F., R.W.A.), Department of Medicine, Emory University School of Medicine, Atlanta, Ga; and the Department of Pharmacology (M.U.-F.), University of Illinois at Chicago, Chicago, Ill.
Correspondence to Masuko Ushio-Fukai, Department of Pharmacology and Center for Lung and Vascular Biology, University of Illinois at Chicago, 835 S Wolcott, M/C 868, E403 MSB, Chicago, IL 60612. E-mail mfukai@uic.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Angiotensin II (Ang II) is a pluripotent hormone in vascular smooth muscle cells (VSMCs) and stimulates arterial hypertrophy, a hallmark of remodeling in hypertension. These effects are mediated primarily through the G protein–coupled receptor Ang II type 1 receptor (AT1R).1 In VSMCs, AT1R-mediated signaling is biphasic, and internalization of the agonist/receptor complex into what we called a "signaling domain" is required for the tonic phase of signaling (initially characterized by phospholipase D activation) but not for the initial phospholipase C stimulation, which occurs at the cell surface.2 This evidence was consistent with the existence of spatially discrete Ang II signaling domains. We showed that sequential Ang II–induced phospholipase activation is mediated through
2 G
subunits (Gq and G12/13), as well as their associated Gß
components.3,4 In addition, various nonreceptor tyrosine kinases, including cAbl and some from the Src family, as well as mitogen-activated protein kinases and Akt, are activated by Ang II and mediate VSMC hypertrophy and growth.5–7 Activation of these pathways is in part dependent on tyrosine phosphorylation (transmodulation) of the epidermal growth factor receptor (EGF-R), which serves as a "scaffold" for the assembly of cSrc and Pyk2, leading to downstream activation of extracellular-regulated kinase (ERK)1/2 and Akt.8,9 These results are consistent with a model that requires temporal dispersion and organization of the AT1R signaling repertoire in VSMCs.7,10
Accumulating evidence suggests that receptors and the signaling molecules with which they associate are not randomly distributed in the cell membrane but are localized in specialized signaling
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