Adenosine2A receptors and epoxyeicosatrienoic acids: a recipe for salt and blood pressure regulation.

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 adenosine2A (A2A) receptors and epoxyeicosatrienoic acids (EETs) is required for the kidneys to respond to increased dietary salt intake.