Recent studies have revealed that an enhancement of sodium-Proton exch
ange is a frequently observed ion transport abnormality in essential h
ypertension. An altered antiport activity not only is measurable in bl
ood cells of hypertensive subjects ex vivo but also is detectable in s
keletal muscle in vivo. Several lines of argument suggest that the alt
ered antiport activity is not an epiphenomenon of hypertension: 1) the
increased activity is found only in a subgroup of patients with high
blood pressure, 2) it is not tightly correlated to the severity or dur
ation of hypertension, and 3) high sodium-proton exchange activity per
sists over time and is not affected by antihypertensive treatment. Ava
ilable evidence suggests that enhanced sodium-proton exchange is assoc
iated with or a cause for the structural alterations found in resistan
ce vessels of hypertensive individuals (media hypertrophy) and left ve
ntricular hypertrophy. This review summarizes some of the physiologica
l properties and roles of the sodium-proton exchanger and discusses it
s kinetic properties in essential hypertension. Furthermore, the reaso
ns for the enhanced antiport activity and its potential implications r
egarding the pathogenesis of hypertension are discussed.