Urinary Na+/K+ ratio has been important in monitoring the daily intake of Na+ and K+. It has also been reported to influence blood pressure changes greater than changes in either Na+ or K+ alone (Kwok et al., 2003; Cook et al., 2009). We have recently reported increased nightime urinary Na+/K+ ratio in humans, which was shown to be dependent on a significant dip in nighttime K+excretion by an aldosterone independent mechanism (Asowata et al., 2016). In the current study, we aimed to investigate if increasing the delivery of Na+ to the distal tubules will alter the previously established dip in nighttime K+ excretion. Ethical approval was obtained for 10 male apparently healthy subjects and we assessed the excretion of aldosterone, Na+ and K+ as well as the Na+/K+ ratio in 12 hour-Day (12h-D) and 12 hour-Night (12h-N) urine samples in control and following furosemide administration. Furosemide was administered to increase the delivery of Na+ to the distal tubule. Control values for the excretion of aldosterone, Na+ and K+in 12h-D (7am-7pm) and 12h-N (7pm-7am) urine samples were collected on the first day. On the following day, 20mg of furosemide was given orally to the subjects twice (7am and 7pm) and 12 hours (Day and Night) urine samples were collected. Na+ and K+ were analyzed using flame photometry while aldosterone concentration was analyzed using the enzyme immunoassay method (DRG International, Inc., USA). Values are expressed as Mean ± SEM and analyzed using Student’s t-test. In control subjects, consistent with a previous report (Asowata et al., 2016), higher Na+/K+ ratio was observed in 12h-N compared with 12h-D urine samples (p<0.01) while aldosterone excretion remained unchanged. Day and night changes in Na+/K+ resulted from a significant difference in urinary K+ excretion, which was lower at night compared with the day urine (p<0.05).Correlation analysis revealed a significant direct relationship between Na+ and K+ in 12h-D (r = 0.82, p<0.01; n = 10) and 12h-N (r = 0.87, p<0.01; n = 10) in controls and after furosemide administration (12h-D; r = 0.97, p<0.001 and 12h-N; r = 0.99, p<0.001; n = 10). However, consistent with our previous finding, no relationships exist between urinary Na+ and K+ with aldosterone in controls and after furosemide. Following the administration of furosemide, urinary Na+/K+ ratio remained significantly higher at night than during the day (p<0.001; n = 10) due to a decrease in urinary K+ excretion at night compared with daytime (p<0.05; n = 10). Even though the administration of furosemide increased aldosterone activity, nighttime dip in K+ excretion was unaffected. Our results support our previous findings that an aldosterone independent mechanism is responsible for the nocturnal fluctuation in urinary potassium excretion.