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

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. Thedelivery of Na+ to the distal nephron is known to be an important determinant of aldosterone mediated secretion of K+ in thissegment of the nephron. Examining the link between distal Na+ delivery and K+ excretion; and how this link affect circadianK+ excretion will advance what is currently known about the maintenance of K+ homeostasis. In the current study, weinvestigated the effect of furosemide-induced increase in distal tubular Na+ on K+ excretion. Na+, K+ and aldosterone levelswere measured in 12-hour day time and 12-hour night time urine samples following furosemide administration, andcompared with controls in 10 apparently healthy male subjects. To confirm the increased delivery of Na+ to the distal nephronby 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 wasunchanged even with increased Na+ delivery to the distal tubules. In healthy individuals, aldosterone increases K+ secretionand this is known to further increase with increased Na+ delivery to the potassium secreting segment of the nephron. Eventhough the administration of furosemide increased aldosterone activity and the delivery of Na+ to the distal tubules, the dipin night time K+ excretion was unchanged. Our findings suggest that the circadian control of K+ excretion is not linked toNa+ levels and thus independent of aldosterone.