Hypertension, Vol 21, 607-617, Copyright © 1993 by American Heart Association
D Rosskopf, R Dusing and W Siffert
Recent studies have revealed that an enhancement of sodium-proton exchange
is a frequently observed ion transport abnormality in essential
hypertension. An altered antiport activity not only is measurable in blood
cells of hypertensive subjects ex vivo but also is detectable in skeletal
muscle in vivo. Several lines of argument suggest that the altered 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 duration of hypertension, and 3)
high sodium-proton exchange activity persists over time and is not affected
by antihypertensive treatment. Available evidence suggests that enhanced
sodium-proton exchange is associated with or a cause for the structural
alterations found in resistance vessels of hypertensive individuals (media
hypertrophy) and left ventricular hypertrophy. This review summarizes some
of the physiological properties and roles of the sodium- proton exchanger
and discusses its kinetic properties in essential hypertension.
Furthermore, the reasons for the enhanced antiport activity and its
potential implications regarding the pathogenesis of hypertension are
discussed.
ARTICLES
Membrane sodium-proton exchange and primary hypertension
Max-Planck-Institut fur Biophysik, Frankfurt/Main, FRG.
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