Dietary potassium loading results in rapid kaliuresis, natriuresis and diuresis associated with reduced phosphorylation (-p) of the distal tubule Na⁺-Cl^- cotransporter (NCC). Decreased NCC-p inhibits NCC mediated Na⁺ reabsorption and shifts Na⁺ downstream for reabsorption by epithelial Na⁺ channels (ENaC) which can drive K⁺ secretion. Whether the signal is initiated by ingesting potassium or a rise in plasma [K⁺] is not understood. We tested the hypothesis, in male rats, that an increase in plasma [K⁺] is sufficient to reduce NCC-p and drive kaliuresis. After an overnight fast, a single 3 hr 2% potassium (2%K) containing meal increased plasma [K⁺] from 4.0±0.1 to 5.2±0.2 mM, increased urinary K⁺, Na⁺, and volume excretion, decreased NCC-p by 60%, and marginally reduced cortical Na⁺-K⁺-2Cl^- cotransporter (NKCC) phosphorylation 25% (P=0.055). When plasma [K⁺] was increased by tail vein infusion of KCl to 5.5±0.1 mM over 3 hr, significant kaliuresis and natriuresis ensued, NCC-p decreased by 60% and STE20/SPS1-related proline alanine-rich kinase (SPAK) phosphorylation was marginally reduced 35% (P=0.052). The following were unchanged at 3 hr by either the potassium-rich meal or KCl infusion: Na⁺/H+ exchanger 3 (NHE3), NHE3-p, NKCC, ENaC subunits, renal outer medullary K⁺ channel. In summary, raising plasma [K⁺] by intravenous infusion to a level equivalent to that observed after a single potassium-rich meal triggers renal kaliuretic and natriuretic responses, independent of K⁺ ingestion, likely driven by decreased NCC-p and activity sufficient to shift sodium reabsorption downstream to where Na⁺ reabsorption and flow drive K⁺ secretion.