Signal transduction mechanisms mediating the physiological and pathophysiological actions of angiotensin II in vascular smooth muscle cells.
By Rhian M. Touyz, E. Schiffrin. Pharmacological Reviews, 2000
953 citations recorded by the source corpus.
Until recently, the signaling events elicited in vascular smooth muscle cells by angiotensin II (Ang II) were considered to be rapid, short-lived, and divided into separate linear pathways, where intracellular targets of the phospholipase C-diacylglycerol-Ca(2+) axis were distinct from those of the tyrosine kinase- and mitogen-activated protein kinase- dependent pathways. However, these major intracellular signaling cascades do not function independently and are actively engaged in cross-talk. Downstream signals from the Ang II-bound receptors converge to elicit complex and multiple responses. The exact adapter proteins or "go-between" molecules that link the multiple intracellular pathways await clarification. Ang II induces a multitude of actions in various tissues, and the signaling events following occupancy and activation of angiotensin receptors are tightly controlled and extremely complex. Alterations of these highly regulated signaling pathways in vascular smooth cells may be pivotal in structural and functional abnormalities that underlie vascular pathological processes in cardiovascular diseases such as hypertension, atherosclerosis, and post-interventional restenosis.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a0b4731071e5dd802169a3fb92551d2dd58a7a88
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In Cardiology and Cardiovascular Medicine
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Citations in the corpus
- Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, neutral): “The role of ROS in signaling has been reviewed extensively (47, 49, 50, 52, 63, 64, 66, 87, 99, 138, 162, 187, 190, 191, 195, 197, 217, 222).”
- Selective COX-1 inhibition: A therapeutic target to be reconsidered. (2010, background): “However, COX-1 blockade improved only in part the Ang II-induced endothelial dysfunction, indicating a residual direct and specific COX-1independent effect of Ang II on the vascular wall [61].”
- The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease (2007, background): “…to support the established premise that most of the vascular and transport actions attributed to the RAS that lead to vascular constriction, enhanced sodium transport, and hypertension are due to the actions of Ang II and also Ang III acting primarily on AT1 receptors (Touyz and Schiffrin, 2000).”
- ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “A cardiovascular hormone, ANG II, signals mainly through the angiotensin type I (AT1) receptor (17, 35, 95, 102, 113).”
- Hydrogen Peroxide: A Signaling Messenger (2006, neutral): “AngII acting through the G-protein coupled AT1 receptor is a major factor stimulating the growth of vascular smooth muscle cells, and many of the pro-growth effects of AngII are believed to be secondary to the activation of MAP kinases (212).”
- Reactive oxygen species in vascular biology: implications in hypertension (2004, neutral): “Non-receptor tyrosine kinases such as Src, JAK2, Pyk2, and Akt, all of which have been implicated in cardiovascular remodeling and vascular damage, are also regulated by ROS (Griendling et al. 2000a; Touyz and Schiffrin 2000; Droge 2001; Touyz et al. 2002b).”
- Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. (2007, background): “The PLC/PLD pathways causing muscle contraction are augmented in hypertensive rats compared with controls, suggesting that alterations in the G protein-activated second messengers may play a role in the pathogenesis of hypertension (9, 194).”