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Potassium Depletion and Salt Sensitivity in Essential Hypertension

Istituto di Semeiotica Medica-Fondazione Don C. Gnocchi-ONLUS and Laboratorio di Informatica e Statistica, Istituto di Pedagogia (M.R.), University of Parma, I 43100 Parma, Italy; and Istituto Scientifico Ospedale S. Luca, IRCCS—Istituto Auxologico Italiano (G.P.), and LaRC-Centro di Bioingegneria, Fondazione Don C. Gnocchi, Politecnico di Milano (M.D.R.), 20148 Milan, Italy

Address all correspondence and requests for reprints to: Paolo Coruzzi, M.D., Unità Cardiovascolare, University of Parma, Fondazione Don Carlo Gnocchi, Piazzale dei Servi 3, I 43100 Parma, Italy. E-mail: paolo.coruzzi{at}unipr.it

Abstract

To evaluate the actual role of potassium depletion on blood pressure, 11 hypertensive patients were placed on a 10-day isocaloric diet providing a daily potassium intake of either 18 or 80 mmol, with each subject serving as his or her own control; the intake of sodium (220 mmol/day) and other minerals was kept constant. On day 11 each patient was also subjected to central volume expansion by water immersion associated with either normal or low potassium intake. After a 10-day period of low potassium intake, systolic blood pressure increased (P < 0.02) by 5 mm Hg, whereas serum potassium decreased (P < 0.001) by 0.9 mmol/L; no significant changes in urinary sodium and a marked increase in urinary calcium excretion (P < 0.001) were found during the 10-day low potassium intake. PRA (P < 0.02) and plasma aldosterone (P < 0.04) concentrations also decreased during low potassium intake in hypertensive patients. Even though an identical natriuretic response was found during the water immersion experiments with either high or low potassium in the whole hypertensive group, the evaluation of hypertensive subjects in relation to salt sensitivity enabled us to disclose pronounced differences in the natriuretic and calciuretic response.

In fact, although an impaired natriuretic ability and moderate calcium loss were particularly found during water immersion in those hypertensive subjects exhibiting a lower salt sensitivity index, a predominant calcium depletion appeared to be the most important consequence of potassium depletion in the hypertensive subjects with a higher salt sensitivity index. By confirming that potassium depletion may exacerbate essential hypertension, our data also suggest that not only sodium restriction, but also potassium and calcium supplementation, could be particularly advisable in salt-sensitive hypertensive patients.

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