<jats:sec><jats:title>Objectives</jats:title><jats:p>To measure the effect of external heating on bladder wall contractile function, histological structure and expression of proteins related to tissue protection and apoptosis.</jats:p></jats:sec><jats:sec><jats:title>Material and Methods</jats:title><jats:p><jats:italic>In vitro</jats:italic> preparations of bladder wall and <jats:italic>ex vivo</jats:italic> perfused pig bladders were heated from 37 to 42°C, 46 and 50°C for 15 min. Isolated preparations were heated by radiant energy and perfused bladders were heated by altering perfusate temperature. Spontaneous contractions or pressure variations were recorded, as well as responses to the muscarinic agonist carbachol or motor nerve excitation <jats:italic>in vitro</jats:italic> during heating. Tissue histology in control and after heating was analysed using haematoxylin and eosin staining and 4′‐6‐diamidino‐2‐phenylindole (<jats:styled-content style="fixed-case">DAPI</jats:styled-content>) nuclear labelling. The effects of heating on protein expression levels of (i) heat shock proteins <jats:styled-content style="fixed-case">HSP</jats:styled-content>27‐<jats:styled-content style="fixed-case">pS</jats:styled-content>er82 and inducible‐<jats:styled-content style="fixed-case">HSP</jats:styled-content>70 and (ii) caspase‐3 and its downstream <jats:styled-content style="fixed-case">DNA</jats:styled-content>‐repair substrate poly‐[<jats:styled-content style="fixed-case">ADP</jats:styled-content>‐ribose] polymerase (<jats:styled-content style="fixed-case">PARP</jats:styled-content>) were measured.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Heating to 42°C reduced spontaneous contractions or pressure variations by ~70%; effects were fully reversible. There were no effects on carbachol or nerve‐mediated responses. Tissue histology was unaffected by heating, and expression of heat shock proteins as well as caspase‐3 and <jats:styled-content style="fixed-case">PARP</jats:styled-content> were also unaltered. A <jats:styled-content style="fixed-case">TRPV</jats:styled-content>1 antagonist had no effect on the reduction of spontaneous activity. Heating to 46°C had a similar effect on spontaneous activity and also reduced the carbachol contracture. Urothelial structure was damaged, caspase‐3 levels were increased and inducible‐<jats:styled-content style="fixed-case">HSP</jats:styled-content>70 levels declined. At 50°C evoked contractions were abolished, the urothelium was absent and heat shock proteins and <jats:styled-content style="fixed-case">PARP</jats:styled-content> expression was reduced with raised caspase‐3 expression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Heating to 42°C caused a profound, reversible and reproducible attenuation of spontaneous activity, with no tissue damage and no initiation of apoptosis pathways. Higher temperatures caused tissue damage and activation of apoptotic mechanisms. Mild heating offers a novel approach to reducing bladder spontaneous activity.</jats:p></jats:sec>