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The extracellular signal-regulated kinase (ERK) pathway: a potential therapeutic target in hypertension

Authors Roberts R

Received 21 April 2012

Accepted for publication 12 June 2012

Published 2 August 2012 Volume 2012:4 Pages 77—83


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Richard E Roberts

School of Biomedical Sciences, University of Nottingham, Nottingham, United Kingdom

Abstract: Hypertension is a risk factor for myocardial infarction, stroke, renal failure, heart failure, and peripheral vascular disease. One feature of hypertension is a hyperresponsiveness to contractile agents, and inhibition of vasoconstriction forms the basis of some of the treatments for hypertension. Hypertension is also associated with an increase in the growth and proliferation of vascular smooth muscle cells, which can lead to a thickening of the smooth muscle layer of the blood vessels and a reduction in lumen diameter. Targeting both the enhanced contractile responses, and the increased vascular smooth muscle cell growth could potentially be an important pharmacological treatment of hypertension. Extracellular signal-regulated kinase (ERK) is a member of the mitogen-activated protein kinase family that is involved in both vasoconstriction and vascular smooth muscle cell growth and this, therefore, makes it an attractive therapeutic target for treatment of hypertension. ERK activity is raised in vascular smooth muscle cells from animal models of hypertension, and inhibition of ERK activation reduces both vascular smooth muscle cell growth and vasoconstriction. This review discusses the potential for targeting ERK activity in the treatment of hypertension.

Keywords: ERK, hypertension, smooth muscle, vasoconstriction

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