Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

Abstract

To clarify the mechanism by which K (KCl) protects against the blood pressure rising action of Na (NaCl), the effects of KCl loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet were studied. Patients (11) 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 < 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 < 0.05) or with changes in cardiac output (P < 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 < 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones. Concomitantly, urinary Na excretion was significantly greater in the early period of NaCl loading in the KCl-supplemented group as compared to the other group. Lower levels of norepinephrine measured in the plasma of the KCl-supplemented patients in the early NaCl-loading phases of the study evidently are indicative of reduced adrenergic neural activity, which might be involved not only in the attenuation of increased cardiac output, but also in the responses of the kidney to shift the pressure-natriuresis relationship toward normal, leading to the natriuresis.