Overactive bladder (OAB) is a highly prevalent disorder associated with increased spontaneous contractions and upregulation of TRPV1 receptors in the bladder mucosa (1). Preliminary data indicates that mild heating suppresses spontaneous contractions. We hypothesised that progressive heating from 37-50oC continuously decreases bladder contractility. We also investigated the role of TRPV channels in this process.For in vitro contractility studies, adult pig bladders of either gender were obtained from a local abattoir and stored in Tyrode’s solution (4oC). Strips with attached mucosa were dissected and superfused with Tyrode’s solution. Isometric contractions were recorded at 37oC or during heating to 42, 46 or 50oC with a heating coil placed above the preparation. The effects of heating were examined in the presence of capsazepine, an antagonist to the TRPV1 agonist, capsaicin. Time controls and reproducibility of heating effects were carried out. Temperature was recorded with thermistor probes in the sub-mucosal space. For ex vivo studies, intact pig bladders with associated vasculature were obtained from a local abattoir and stored in Kreb’s solution (4oC). The bladders were maintained under physiological conditions in a heated organ bath and perfused with Krebs buffer. The lumen was filled via a urethral catheter with Kreb’s solution (both at 37 or 42oC). Intravesical pressure was measured with a double-lumen catheter via a ureter. Temperature was recorded with thermistor probes in the bladder lumen. In both studies spontaneous contraction amplitude, duration, and frequency as well as area under the curve (AUC) were measured for 10 min periods at the end of control or heating periods. Data are mean±SEM and the null hypothesis was rejected at p<0.05 using ANOVA.In vitro, heating to 42oC reduced AUC (59.0±9.6%, p<0.05) and amplitude (88.9±7.2%) of spontaneous contractions (37oC=100%). Heating to 46oC had no effect on AUC (128 ± 7.2%) but enhanced the amplitude (225.2±23.9%, p<0.01). Heating to 50oC enhanced both AUC (250.0±36.0%, p<0.05) and amplitude (519.0±62.0%, p<0.01). Contraction duration spontaneous was reduced and frequency was increased at all temperatures. All changes were fully reversible on return to 37°C (n=7). Capsazepine abolished the effect of heating to 42oC on AUC (99.3±23.5%) and amplitude (150.4±40.4%) but not on duration or frequency (n=10). I Ex vivo heating to 42oC reduced the AUC (55.1±9.5%, p<0.05) and duration (58.9±9.2%, p<0.05) but did not affect amplitude (95.1±11.2%); frequency was increased (176.6±21.7%, p=0.05; n=5).Different contractile responses to mild (42oC) or greater (46, 50oC) heating were observed. The greatest suppression of spontaneous contractions was at 42oC in isolated preparations and perfused bladders. This reduction could be mediated in part through TRPV1 channels.