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(Hypertension. 2008;51:1449.)
© 2008 American Heart Association, Inc.

Brief Reviews

G Protein–Coupled Receptor Kinase 4

Role in Blood Pressure Regulation

Chunyu Zeng; Van Anthony M. Villar; Gilbert M. Eisner; Scott M. Williams; Robin A. Felder; Pedro A. Jose

From the Department of Cardiology (C.Z.), Daping Hospital, Third Military Medical University, Chongqing, People’s Republic of China; Departments of Pediatrics (V.A.M.V., P.A.J.), Internal Medicine (G.M.E.), and Physiology and Biophysics (P.A.J.), Georgetown University Medical Center, Washington, DC; Division of Cardiovascular Medicine (S.M.W.), Vanderbilt University Medical Center, Nashville, Tenn; Department of Pathology (R.A.F.), Virginia University for the Health Sciences, Charlottesville, Va.

Correspondence to Chunyu Zeng, Department of Cardiology, Daping Hospital, Third Military Medical University, Chongqing City, People’s Republic of China. E-mail cyzeng1@hotmail.com

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Nearly 30% of middle-aged Americans have hypertension, but the prevalence is higher in non-Hispanic blacks and individuals >60 years of age (65%).¹ There is a direct and quantitative relationship between higher blood pressure values and mortality. Although 30% to 50% is thought to be heritable, the genetic cause(s) of essential hypertension has been difficult to identify. More than 1 gene is undoubtedly involved, because Mendelian dominant and recessive traits are not readily discernible in hypertensive subjects, except in those with monogenic forms of hypertension. Moreover, in any hypertensive individual, risk-predisposing genes are engaged in a complex network of gene-gene and gene-environment interactions.^2,3

The kidney plays a major role in the long-term regulation of blood pressure, and abnormal sodium chloride metabolism is frequently encountered in hypertension. Therefore, many studies have focused on the abnormal renal handling of sodium chloride in the pathogenesis of essential hypertension.^2,4 Approximately 50% of subjects with essential hypertension are sodium chloride sensitive.⁵ Indeed, humans with salt-sensitive hypertension have increased sodium transport in the renal proximal tubule and medullary thick ascending limb, although distal tubular mechanisms may also be involved.⁶ The sodium retention in hypertension is because of enhanced sodium transport, per se, and/or a failure to respond appropriately to signals that decrease sodium transport. Sodium transport is regulated by natriuretic and antinatriuretic hormones and humoral agents, such as dopamine and angiotensin, which exert their effects via G protein–coupled receptors (GPCRs). Activation of certain postjunctional dopamine receptor subtypes (D₁R, D₃R, D₄R, and D₅R) and . . . [Full Text of this Article]

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