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(Hypertension. 2009;54:1223.)
© 2009 American Heart Association, Inc.

Editorial Commentaries

Adenosine_2A Receptors and Epoxyeicosatrienoic Acids

A Recipe for Salt and Blood Pressure Regulation

John D. Imig

From the Department of Pharmacology and Toxicology, Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wis.

Correspondence to John D. Imig, Department of Pharmacology and Toxicology, Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI 53226. E-mail jdimig@mcw.edu

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

	Introduction

 
Salt has been used as a food preservative and part of the human diet for thousands of years. Consequently, human dietary sodium chloride intake is significantly higher than that needed to sustain life. Fortunately, kidneys function to regulate sodium chloride excretion to maintain proper levels of sodium chloride and extracellular volume when dietary salt intake changes. If the kidneys are properly functioning, then an increase in dietary salt intake results in increased sodium chloride excretion (natriuresis), and extracellular fluid volume remains unchanged. On the other hand, if the kidneys do not function properly to excrete sodium chloride, then extracellular fluid volume expansion occurs, and an elevation in blood pressure is required to bring extracellular fluid volume and plasma sodium back to homeostatic levels.

The report by Liclican et al¹ in this issue of Hypertension provides convincing evidence that a properly functioning axis that includes adenosine_2A (A_2A) receptors and epoxyeicosatrienoic acids (EETs) is required for the kidneys to respond to increased dietary salt intake.

	A2A Receptors and EETs: Dietary Salt and Blood Pressure

 
A balance between salt intake and salt excretion is maintained by a coordinated effort that relies heavily on proper kidney function. When dietary salt intake is increased, there are neural, hormonal, and paracrine factors, as well as the proper function of renal blood vessels and tubular epithelial cell transporters, working in unison to excrete the excess salt. EETs have been demonstrated to be an essential component of this coordinated renal natriuretic response. High dietary salt has been demonstrated to increase renal cytochrome P450 2C (CYP2C) enzymes . . . [Full Text of this Article]

Related Article:

Inhibition of the Adenosine_2A Receptor-Epoxyeicosatrienoic Acid Pathway Renders Dahl Salt-Resistant Rats Hypertensive

Elvira L. Liclican, Anabel B. Doumad, Jianjin Wang, Jing Li, John R. Falck, Charles T. Stier, Jr, and Mairéad A. Carroll
Hypertension 2009 54: 1284-1290. [Abstract] [Full Text] [PDF]