Hypertension, Vol 6, 184-192, Copyright © 1984 by American Heart Association
T Fujita and K Ando
To clarify the mechanism by which potassium (KCl) protects against the
blood pressure rising action of sodium (NaCl), we studied the effects of
KCl loading in patients with idiopathic hypertension who, after a period of
NaCl restriction, partook of a high NaCl diet. Eleven patients who had
taken the KCl supplement (96 mEq/day) during the high NaCl period showed
lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25
to 250 mEq/day than 12 patients who had not taken the KCl supplement (p
less than 0.001). With a high NaCl diet, the KCl-supplemented patients
retained less NaCl, gained less weight, and showed a lesser increase in
plasma volume and cardiac output than the non-KCl-supplemented ones.
Overall, the increase in blood pressure levels during the high Na diet
correlated directly either with changes in plasma volume (p less than 0.05)
or with changes in cardiac output (p less than 0.01). The results suggest
that KCl may prevent a rise in blood pressure with NaCl loads in
hypertensive patients by attenuating the increase in cardiac output, mainly
as a result of the natriuresis. Furthermore, plasma norepinephrine was
measured to estimate the sympathetic activity, since the sympathetic
nervous system is known to control urinary NaCl excretion. From the low
NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was
significantly (p less than 0.01) decreased in the KCl-supplemented
patients, whereas it remained unchanged in the non-KCl-supplemented
ones.(ABSTRACT TRUNCATED AT 250 WORDS)
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Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives
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