Five primary prostanoids are synthesized by the cyclooxygenase enzymes, COX-1 and COX-2: the prostaglandins PGE(2), PGF(2α), PGI(2), PGD(2) and thromboxane A2. High levels of these signaling molecules have been implicated--in both animal models and human studies--in decreased functional bladder capacity and micturition volume and increased voiding contraction amplitude. Thus, inhibition of prostanoid production or the use of prostanoid receptor antagonists, might be a rational way to treat patients with detrusor muscle overactivity. Similarly, prostanoid receptor agonists, or agents that stimulate their production, might have a function in treating bladder underactivity. Although some promising results have been reported, the adverse effects of nonselective cyclooxygenase inhibitors are a major concern that restricts their use in the treatment of functional bladder disorders. Further preclinical and clinical studies are needed before cyclooxygenase inhibitors, prostanoid receptor agonists and antagonists become worthwhile therapeutic tools in this setting.