We previously showed that ambient urine osmolality was higher in TNF deficient mice compared with age‐ and sex‐matched wild type (WT) mice. As the role of TNF in the kidney is still being defined, effects of renal‐specific TNF silencing on renal Na(+)‐K(+)‐2Cl(‐) cotransporter (NKCC2) and aquaporin‐2 (AQP2) expression was determined. Six days after intrarenal injection of lentivirus construct EGFP‐TNF‐ex4 into both kidneys of WT mice, renal but not splenic TNF mRNA levels were significantly reduced. Injection of control lentivirus (U6) did not alter TNF mRNA in either kidney or spleen. EGFP‐TNF‐ex4, but not U6, also increased NKCC2A mRNA levels in renal outer medulla and inner medullary AQP2 mRNA and protein expression. Urine osmolality increased in mice injected with EGFP‐TNF‐ex4 compared with those injected with U6, suggesting that the increase in NKCC2 and AQP2 due to renal silencing of TNF contributed to an increase osmolality. As TNF production by the TAL was induced by administration of 1% NaCl in the drinking water for 3 days, the effects of TNF silencing on urine volume were determined. Mice were acclimated in metabolic cages for 3 days after receiving intrarenal injections of either EGFP‐TNF‐ex4 or U6. Food, body weight, water intake, and urine output was then measured in mice given 1% NaCl or tap water for 3 days. Both water intake and urine output were reduced in mice injected with EGFP‐TNF‐ex4 compared with mice given U6 lentivirus. The decrease in urine volume was associated with an increase in NKCC2A and AQP2 mRNA accumulation. Collectively, these findings suggest that TNF produced by the kidney inhibits transporter expression and regulates responses to high NaCl intake.