Circadian Potassium Excretion is Unaffected Following Furosemide Induced Increase in Sodium Delivery to the Distal Nephron

B P Ilenwabor, E O Asowata, L F Obika

Abstract


The mineralocorticoid aldosterone is widely accepted as a key regulator of K+ balance as well as urinary K+
excretion. However, recent evidence suggests that the circadian control of K+ excretion is independent of aldosterone. The
delivery of Na+ to the distal nephron is known to be an important determinant of aldosterone mediated secretion of K+ in this
segment of the nephron. Examining the link between distal Na+ delivery and K+ excretion; and how this link affect circadian
K+ excretion will advance what is currently known about the maintenance of K+ homeostasis. In the current study, we
investigated the effect of furosemide-induced increase in distal tubular Na+ on K+ excretion. Na+, K+ and aldosterone levels
were measured in 12-hour day time and 12-hour night time urine samples following furosemide administration, and
compared with controls in 10 apparently healthy male subjects. To confirm the increased delivery of Na+ to the distal nephron
by furosemide, increased Na+ excretion and aldosterone activity was observed in subjects administered furosemide.
Consistent with previous reports, night time K+ excretion was significantly lower than day time, and this observation was
unchanged even with increased Na+ delivery to the distal tubules. In healthy individuals, aldosterone increases K+ secretion
and this is known to further increase with increased Na+ delivery to the potassium secreting segment of the nephron. Even
though the administration of furosemide increased aldosterone activity and the delivery of Na+ to the distal tubules, the dip
in night time K+ excretion was unchanged. Our findings suggest that the circadian control of K+ excretion is not linked to
Na+ levels and thus independent of aldosterone

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