Introduction and objective: Caveolin-1- deficiency leads to urogenital alterations in males. Whether contractile changes in the male bladder are secondary to outflow obstruction caused by a hypertrophic prostate or reflect a role of caveolae in detrusor signaling is not known. This was addressed by characterising detrusor contractility in wild type (WT) and caveolin-1-deficient (KO) female mice. Methods: Detrusors from 32-week-old KO and WT female mice were examined in vitro using myography. Length- tension relationships were generated and contractility was determined at L₀. Western blotting was used to assess contents of caveolar proteins and muscarinic M₃ receptors. Results: KO mice consumed significantly less water per day. The bladder weight was not changed. Depolarisation-induced contraction was suppressed at L₀, as was the scopolamine sensitive component of nerve- induced twitches. Carbachol-induced stress was reduced at intermediate carbachol concentrations, but E_max force was increased relative to KCl-contraction. M₃ receptor expression was increased in KO detrusor. Conclusions: Genetic ablation of caveolae in the female mouse leads to substantial functional changes in the bladder, ruling out prostate hypertrophy as a contributing factor. Caveolae facilitate muscarinic signalling in the detrusor, but adaptation, involving increased expression of M ₃ receptors, allows control levels of stress to be approached at intense neural activity.