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BioMed Research International
Volume 2014 (2014), Article ID 182862, 6 pages
Research Article

Effect of Inflammatory Mediators on ATP Release of Human Urothelial RT4 Cells

Graduate School of Medicine, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW 2522, Australia

Received 28 February 2014; Accepted 2 April 2014; Published 15 April 2014

Academic Editor: Gilho Lee

Copyright © 2014 Kylie J. Mansfield and Jessica R. Hughes. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Inflammation is an important contributor to the aetiology of a number of bladder dysfunctions including interstitial cystitis, painful bladder syndrome, and overactive bladder. The aim of this study was to examine the effects of inflammatory mediators on urothelial ATP release. Human urothelial RT4 cells were exposed to normal buffer or varying concentrations of inflammatory mediators (bradykinin, histamine, and serotonin) in the presence or absence of hypotonic stretch stimuli (1 : 2 dilution of Krebs-Henseleit buffer). Others have demonstrated that bradykinin increased stretch-induced ATP release; however, we observed no change in control or stretch-induced ATP release with bradykinin. Pretreatment of RT4 cells with histamine or serotonin decreased stretch-induced ATP release ( , , resp.). Previous studies have demonstrated increased ATP release in response to inflammation utilising whole bladder preparations in contrast to our simple model of cultured urothelial cells. The current study suggests that it is unlikely that there is a direct interaction between the release of inflammatory mediators and increased ATP release, but rather more complex interactions occurring in response to inflammation that lead to increased bladder sensation.