Hypertension, Vol 6, 152-158, Copyright © 1984 by American Heart Association
F Skrabal, H Herholz, M Neumayr, L Hamberger, M Ledochowski, H Sporer, H Hortnagl, S Schwarz and D Schonitzer
If high sodium intake is involved in the pathogenesis of essential
hypertension, the effects of changing the sodium intake should be
demonstrable in the susceptible part of the normotensive population.
Therefore, we have investigated the effects of moderate salt restriction in
52 young normotensive subjects with and without a family history of
hypertension; 22 (42%) responded to moderate salt restriction (200 to 50
mmol/day) over 2 weeks, with a significant fall in blood pressure shown by
continuous automatic blood pressure recordings. Accordingly, these subjects
were classified as salt- sensitive, and the remainder as salt-resistant.
Compared to salt- resistant subjects, salt-sensitive subjects showed a
2.5-fold higher incidence of a positive family history of hypertension (p
less than 0.01), and a significantly higher blood pressure and lower
salivary sodium concentration during the usual high sodium diet. Although
there were no differences in Na,K-ATPase activity and in Na-K cotransport
of erythrocytes, the pressor response to infused norepinephrine in salt-
sensitive subjects was double that of salt-resistant subjects independent
of the diet and this was linked to indirect evidence for enhanced proximal
tubular sodium reabsorption. On the usual high sodium diet, 40% of the
normal population may be salt-sensitive and prone to develop hypertension.
Hypersensitivity to catecholamines (genetically determined?) may be the
cause of salt sensitivity. A low sodium concentration in saliva deserves
further study as a simple screening test to identify salt-sensitive
subjects.
ARTICLES
Salt sensitivity in humans is linked to enhanced sympathetic responsiveness and to enhanced proximal tubular reabsorption
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