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Urothelial cells have been implicated in bladder mechanosensory transduction, and thus, initiation of the micturition reflex. Cell deformation caused by tension forces at an air-liquid interface (ALI) can induce an increase in intracellular Ca 2+  concentration ([Ca 2+ ] i ) and ATP release in some epithelial cells. In this study, we aimed to examine the cellular mechanisms underlying ALI-induced [Ca 2+ ] i  increase in cultured urothelial cells. The ALI was created by stopping the influx of the perfusion but maintaining efflux. The [Ca 2+ ] i  increase was measured using the Ca 2+  imaging method. The ALI evoked a reversible [Ca 2+ ] i  increase and ATP release in urothelial cells, which was almost abolished by GdCl 3 . The specific antagonist of the transient receptor potential vanilloid (TRPV4) channel (HC0674) and the antagonist of the pannexin 1 channel ( 10 panx) both diminished the [Ca 2+ ] i  increase. The blocker of Ca 2+ -ATPase pumps on the endoplasmic reticulum (thapsigargin), the IP3 receptor antagonist (Xest-C), and the ryanodine receptor antagonist (ryanodine) all attenuated the [Ca 2+ ] i  increase. Degrading extracellular ATP with apyrase or blocking ATP receptors (P2X or P2Y) with pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) significantly attenuated the [Ca 2+ ] i  increase. Our results suggest that both Ca 2+  influx  via  TRPV4 or pannexin 1 and Ca 2+  release from intracellular Ca 2+  stores  via  IP3 or ryanodine receptors contribute to the mechanical responses of urothelial cells. The release of ATP further enhances the [Ca 2+ ] i  increase by activating P2X and P2Y receptors  via  autocrine or paracrine mechanisms.

Cell Deformation at the Air-Liquid Interface Evokes Intracellular Ca2+ Increase and ATP Release in Cultured Rat Urothelial Cells