Purpose: Previous studies found that two potassium channel proteins, ROMK (renal outer medullary K+ channel) and KCNQ1 (voltage-gated K+ channel 7.1) exist in the bladder epithelium. ROMK channel is predominantly located on the apical membrane; KCNQ1 channel is essential for recycling potassium across the basolateral membrane of epithelial cells. Both potassium channels have never been studied the compensatory mechanism of the increased potassium leakage in patients with interstitial cystitis/painful bladder syndrome.
Materials and Methods: The study group consisted of 24 patients with IC/PBS, and the control group consisted of 12 volunteers without any IC/PBS symptoms. Bladder biopsies were taken from both groups, respectively. We determined expression and distribution of potassium channels using immunoblotting, immunohistochemistry, and immunofluorescent staining under confocal laser microscopy. Data were analyzed using the Students t -test.
Results: The protein abundance of ROMK in study group was significantly higher (3.3-fold) than in the control group and it predominantly expressed in apical cells of bladder urothelium under confocal microscopy. In contrast, there was no different expression of KCNQ1 in either groups and it located over whole basolateral membrane by confocal microscopy.
Conclusion: Our data showed that the increased expression of ROMK protein in apical cells of the bladder urothelium in IC/PBS patients. It would seem that through the upregulation of ROMK channel to permit avid potassium flux into bladder lumen to keep intracellular K+ homeostasis of dysfunctional bladder urothelium.