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Symposium Report |
1 Canadian Institutes for Health Research Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada
Abstract
Resistance arteries undergo structural changes (vascular remodelling) in hypertension. These changes involve media thickening, reduced lumen diameter and consequent increased media:lumen ratio. Cellular processes underlying these events include altered vascular smooth muscle cell (VSMC) growth, migration, differentiation and increased extracellular matrix abundance. Another factor contributing to remodelling is inflammation, associated with macrophage infiltration, fibrosis and increased expression of redox-sensitive pro-inflammatory genes. Among the factors involved in arterial remodelling, angiotensin (Ang) II appears to be one of the most important. Ang II, a multifunctional peptide with pleiotropic actions, modulates vasomotor tone, cell growth, apoptosis/anoikis, cell migration and extracellular matrix deposition. It is pro-inflammatory and it stimulates production of growth factors and vasoactive agents. The multiple actions of Ang II are mediated via complex intracellular signalling pathways including stimulation of the phosholipase C (PLC)–inositol 1,4,5-trisphosphate (IP3)–1,2-diacylglycerol (DAG) cascade, mitogen-activated protein (MAP) kinases, tyrosine kinases and RhoA/Rho kinase. Furthermore, Ang II elicits many of its (patho)physiological effects by stimulating reactive oxygen species (•O2– and H2O2) generation through activation of vascular NAD(P)H oxidase. •O2– and H2O2 in turn influence downstream signalling molecules including transcription factors, tyrosine kinases/phosphatases, Ca2+ channels and MAP kinases. Interaction between these systems is complex and dysregulation at any level may contribute to vascular remodelling. Targeting such molecules/pathways could prevent or induce regression of hypertensive vascular damage thereby ameliorating development of hypertension and preventing target organ damage. The present review discusses the role of Ang II in remodelling of resistance arteries, focusing on some signalling pathways involved in vascular growth and inflammation in hypertension.
(Received 1 April 2005;
accepted after revision 10 May 2005; first published online 12 May 2005)
Corresponding author R. Touyz: Canada Research Chair in Hypertension, Kidney Research Centre, Ottawa Health Research Institute/University of Ottawa, Room 1333A, 451 Smyth Road, Ottawa, K1H 8M5, Ontario, Canada. Email: rtouyz{at}uottawa.ca
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