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⁺ concentration ([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-h 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 h, 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 h by either the potassium-rich meal or KCl infusion: Na⁺/H⁺ exchanger 3 (NHE3), NHE3-p, NKCC, ENaC subunits, and 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.