Prostaglandin E₂(PGE₂) activates its receptors on the renal collecting duct (CD) to stimulate renal Na⁺ and water excretion. The PG carrier PGT is expressed on the CD apical membrane, where it mediates PG reuptake as part of the termination of autacrine PG signaling. We tested the hypothesis that dietary salt loading regulates PGT gene transcription in renal CDs. We placed Green Fluorescence Protein (GFP) under control of 3.3 kb of the mouse PGT promoter and injected this construct into the pronuclei of fertilized FVB mouse eggs. Four of 38 offspring were GFP-positive by genotyping. We extensively characterized one (#29) PGT-GFP transgenic mouse line. On microscopic examination, GFP was expressed in CDs as determined by their expression of aquaporin-2. We fed mice a low (0.03% NaCl), normal (0.3% NaCl), or high (3% NaCl) salt diet for two weeks and quantified CD GFP expression. The average number of GFP-positive CD cells per microscopic section varied directly with dietary salt intake. Compared to mice on the control (0.3% sodium) diet, mice on a low (0.03%) sodium diet had reduced numbers of GFP-positive cells (71% of control, p < 0.001) whereas mice on a high (3%) sodium diet had increased numbers of GFP-positive cells (139% of control, p < 0.001). This increase in apparent collecting duct PGT transcription resulted in a 51-55% increase (p < 0.001) in whole kidney PGT mRNA levels as determined by real-time PCR. Regulation of PG signal termination via reuptake represents a new pathway for controlling renal Na⁺ balance.