G Protein-coupled receptor kinase 4: Role in hypertension

4^th International Conference on Nephrology & Therapeutics

September 14-16, 2015 Baltimore, USA

Pedro A Jose1, Jian Yang2, Van Anthony M Villar1 and Chunyu Zeng2

1University of Maryland, USA 2The Third Military Medical University, P.R. China

Posters-Accepted Abstracts: J Nephrol Ther

Abstract :

G protein-coupled receptors (GPCRs) mediate cellular responses to a myriad of hormones and neurotransmitters, playing a vital role in the regulation of physiological processes, including blood pressure. The dopaminergic and renin-angiotensin systems interact to regulate blood pressure. Dopamine and angiotensin II (Ang II) exert their effects via GPCRs, with the ultimate effect of keeping the balance of sodium excretion and vasoconstriction and the long-term control of blood pressure. G protein-coupled receptor kinases (GRKs) are essential for terminating the signaling of agonist-bound GPCRs through initiation of receptor desensitization. Abnormal GRK4 function has the potential to affect GPCR (such as dopamine receptors and Ang II type 1 receptor (AT1R))-regulated biological responses in many pathological conditions, such as hypertension. Both in vivo and in vitro studies show that constitutively active GRK4 variants (R65L, A142V, and A486V) play a crucial role in regulating function of dopamine receptors and AT1R, are involved into the pathogenesis of hypertension. Moreover, genetic studies also show that in several ethnic groups, GRK4 gene variants are associated with essential hypertension and/or salt-sensitive hypertension, blood pressure response to antihypertensive medicines, and adverse cardiovascular outcomes of antihypertensive treatment.

Biography :

Email: pjose@medicine.umaryland.edu