Prostate inflammation (PI) is a clinical condition associated with infection and/or inflammation of the prostate. It is a common disease frequently associated to lower urinary tract (LUT) symptoms. The urethra is an understudied structure in the LUT and plays a fundamental role in the urinary cycle. Here we propose to evaluate the effect of PI on the urethra tissue. Male Sprague-Dawley rats were used and PI was induced by formalin injection into the ventral lobes of the prostate. Pelvic urethra at the prostatic level was harvested for histological analysis, contraction (Electrical-field stimulation, phenylephrine) and relaxation (Sodium nitroprusside/MK-571) experiments. Various gene targets (MTCO2,TGFB1,IL1B,HIF1A,ADRA1A,ITPR1,CACNA1D,NOS2, GUCY1B2,PDE5A,PRKG1 and ABCC5) were quantified and cGMP level measured. No histological changes were detected, and functional assays revealed decreased contraction and increased relaxation of the PI group urethra. MK-571 addition to functional assays increased urethral relaxation. Genes associated to inflammation were up-regulated in the PI group urethra, such as COX2, TGFβ1, IL1β and HIF1α. We also found increased expression of L-type Ca2+ channel and nNOS enzyme and decreased expression of the MRP5 pump. Lastly, cGMP production was enhanced in the urethral tissue of PI animals. Results indicate that PI is associated with proinflammatory gene expression in the urethra without histologically evident inflammation and that PI produces a dysfunctional urethra and MRP5 pump down-regulation, which results in cGMP accumulation inside the cell. These findings would help to better understand LUT dysfunctions associated with PI and the role of MRP pumps in the control of LUT function.