RESUMO
AIMS: To highlight novel experimental approaches that test if the Myogenic Hypothesis remains viable as a contributor to the aetiology of detrusor overactivity. METHODS: To summarise the conclusions of a workshop held under the auspices of ICI-RS in 2013. RESULTS: Several theories may explain the pathology of detrusor overactivity and include a myogenic theory with fundamental changes to detrusor muscle excitation-contraction coupling. The isolated bladder displays micromotions that do not normally translate into significant changes of intravesical pressure. However, their amplitude and frequency are altered in animal models of bladder dysfunction. The origin of micromotions, if they generate significant changes of intravesical pressure and contribute to urinary tract sensations remain unanswered. Within the myocyte, changes to contractile protein phosphorylation through accessory proteins and cytoplasmic regulatory pathways occur in lower urinary tract pathologies associated with detrusor overactivity. Furthermore, myocytes isolated from overactive human bladders generate greater spontaneous activity, but a complete description of changes to ionic currents remains to be characterised. Finally, several growth factors, including mechano-growth factor, are released when bladder wall stress is increased, as with outflow obstruction. However the phenotype of the transformed detrusor myocytes remains to be measured. CONCLUSIONS: A number of lines of evidence suggest that the Myogenic Hypothesis remains viable as a contributor to detrusor overactivity.
