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Defective vasodilatory mechanisms in hypertension: a G-protein-coupled receptor perspective

Defective vasodilatory mechanisms in hypertension: a G-protein-coupled receptor perspective Defective vasodilatory mechanisms in hypertension: a G-protein- coupled receptor perspective Ross D. Feldman and Robert Gros Abbreviations Purpose of review The purpose of this article is to review recent evidence cAMP cyclic AMP eNOS endothelial nitric oxide synthase relating to the regulation of vasodilatation and alterations in GPCR G-protein-coupled receptor these mechanisms in the hypertensive state. In particular, GRK G-protein-coupled receptor kinase NOS nitric oxide synthase we will focus on signaling systems regulating nitric oxide PI3K phosphatidylinositol 3 -kinase synthase and intracellular cyclic AMP – the two principal PKA protein kinase A RGS regulator of G-protein signaling mechanisms mediating vasodilatation. SNP single-nucleotide polymorphism Recent findings G-protein-coupled-receptor-mediated, endothelial- 2006 Lippincott Williams & Wilkins dependent processes are increasingly being seen as 1062-4821 critical vasodilatory mechanisms. Impairment of endothelial responses to G-protein-coupled receptor activation is a key component of the decrease in G-protein-coupled-receptor- Introduction mediated vasodilatation in hypertension. In addition, an A mosaic of neural, hormonal and cellular abnormalities ‘uncoupling’ of the G-protein-coupled receptor/G-protein have been described as being associated with the hyper- complex is the principal mechanism underlying impaired tensive state, many or all of which may play a role in the G-protein-coupled-receptor-mediated vasodilatation in pathogenesis and maintenance of hypertension. It http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in Nephrology & Hypertension Wolters Kluwer Health

Defective vasodilatory mechanisms in hypertension: a G-protein-coupled receptor perspective

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ISSN
1062-4821
eISSN
1473-6543
DOI
10.1097/01.mnh.0000214772.96361.ef
pmid
16481879
Publisher site
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Abstract

Defective vasodilatory mechanisms in hypertension: a G-protein- coupled receptor perspective Ross D. Feldman and Robert Gros Abbreviations Purpose of review The purpose of this article is to review recent evidence cAMP cyclic AMP eNOS endothelial nitric oxide synthase relating to the regulation of vasodilatation and alterations in GPCR G-protein-coupled receptor these mechanisms in the hypertensive state. In particular, GRK G-protein-coupled receptor kinase NOS nitric oxide synthase we will focus on signaling systems regulating nitric oxide PI3K phosphatidylinositol 3 -kinase synthase and intracellular cyclic AMP – the two principal PKA protein kinase A RGS regulator of G-protein signaling mechanisms mediating vasodilatation. SNP single-nucleotide polymorphism Recent findings G-protein-coupled-receptor-mediated, endothelial- 2006 Lippincott Williams & Wilkins dependent processes are increasingly being seen as 1062-4821 critical vasodilatory mechanisms. Impairment of endothelial responses to G-protein-coupled receptor activation is a key component of the decrease in G-protein-coupled-receptor- Introduction mediated vasodilatation in hypertension. In addition, an A mosaic of neural, hormonal and cellular abnormalities ‘uncoupling’ of the G-protein-coupled receptor/G-protein have been described as being associated with the hyper- complex is the principal mechanism underlying impaired tensive state, many or all of which may play a role in the G-protein-coupled-receptor-mediated vasodilatation in pathogenesis and maintenance of hypertension. It

Journal

Current Opinion in Nephrology & Hypertension – Wolters Kluwer Health

Published: Mar 1, 2006

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