This study investigates whether in a magnesium-deficient state, the administration of an amiloride bolus can cause an increase in magnesium absorption in the distal convoluted tubule when compared to a magnesium-replete state. Additionally, the impact if magnesium on NCC activity was investigated. The amiloride response experiment helped support the conclusion that a low magnesium state causes increased urinary potassium excretion, likely through a combination of NCC inhibition and ROMK disinhibition. The magnesium reversal experiment supports the conclusion that no permanent tubular damage occurs to the distal nephron affecting NCC expression. Further studies are necessary to better understand the complex relationships between magnesium, potassium, and sodium management by NCC, ROMK, and ENaC in the distal nephron.