Table 1.

Summary of the overall effects of genotype and lithium on Na⁺ and K⁺ transporters along the nephron

	Results of Two-Way ANOVA
Transporter/Channel	Effect of P2Y2R KO	Effect of lithium
NHE3
Cortex	⇆	⇆
Medulla	↓	⇆
α1-Na+-K+-ATPase
Cortex	⇆	⇆
Medulla	↓	⇆
NaPi-2
Cortex	⇆	↓
NCC
Cortex	↓	↑
NKCC2
Cortex	↓	⇆
Medulla	↑	⇆
α-ENaC
Cortex	↓	⇆
Medulla	↓	↓
β-ENaC
Cortex	↓	↑↓*
Medulla	⇆	↓
γ-ENaC
Cortex	⇆	↑↓*
Medulla	⇆	↓*
ROMK
Cortex	↑	⇆
Medulla	⇆	⇆
BK
Cortex	⇆	⇆
Medulla	⇆	⇆*

Significant (P < 0.05) two-way ANOVA findings are shown as an increase (↑), a decrease (↓), or no change (⇆).

NHE3, Na⁺/H⁺ exchanger type 3; NaPi-2, Na⁺-P_i cotransporter type 2; NCC, Na⁺-Cl⁻ cotransporter; NKCC2, Na⁺-K⁺-2Cl⁻ cotransporter 2; ENaC, epithelial Na⁺ channel; ROMK, renal outer medullary K⁺ channel; BK, large-conductance K⁺ channel.

^*Significant interaction. In the case of cortical β- and γ-ENaC and medullary BK channels, the means increased with lithium in wild-type mice and decreased with lithium in P2Y₂ receptor (P2Y₂R) knockout (KO) mice. For medullary γ-ENaC, abundance was decreased in both wild-type and KO mice, but to a significantly greater extent in KO mice.