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TRP channels in hypertension

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ELSEVIER
DOI: 10.1016/j.bbadis.2007.02.009

Keywords

pulmonary arterial hypertension; essential hypertension; transient receptor potential channels; ca(2+); proliferation

Funding

  1. NHLBI NIH HHS [R01 HL064945-08, HL 054043, R29 HL054043, R01 HL066012-06, HL 064945, HL 066012, R01 HL054043-12, R01 HL064945, R01 HL054043, R01 HL066012] Funding Source: Medline

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Pulmonary and systemic arterial hypertension are associated with profound alterations in Ca2+ homeostasis and smooth nriuscle cell proliferation. A novel class of non-selective cation channels, the transient receptor potential (TRP) channels, have emerged at the forefront of research into hypertensive disease states. TRP channels are identified as molecular correlates for receptor-operated and store-operated cation channels in the vasculature. Over 10 TRP isoforms are identified at the mRNA and protein expression levels in the vasculature. Current research implicates upregulation of specific TPP isoforms to be associated with increased Ca2+ influx, characteristic of vasoconstriction and vascular smooth muscle cell proliferation. TRP channels are implicated as Ca (2+) entry pathways in pulmonary hypertension and essential hypertension. Caveolae have recently emerged as membrane microdomains in which TRP channels may be co-localized with the endoplasmic reticulum in both smooth muscle and endothelial cells. Such enhanced expression and function of TRP channels and their localization in caveclae in pathophysiological hypertensive disease states highlights their importance as potential targets for pharmacological intervention. (c) 2007 Elsevier B.V. All rights reserved.

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