Cellular Sodium Transport in Essential Hypertension

Abstract

The idea that hypertension might be associated with alterations in the small intracellular pool of sodium can be traced back to 1952, when Tobian and Binion reported that the sodium content of renal arteries, as measured during postmortem examination, was increased in hypertensive subjects as compared with normotensive controls.¹ This early observation highlights the central problem associated with the study of sodium transport in hypertension, in that it represents an attempt to examine directly the tissue most obviously involved in the mechanism of hypertension — vascular smooth muscle — while demonstrating the difficulty of obtaining valid estimates of the sodium . . .