Autonomous wave activity occurs in the decentralized bladder and may contribute to upper tract damage and incontinence. In order to clarify the poorly understood pathophysiology and neuropharmacology of autonomous waves, cats were prepared with L7-S3 ventrodorsal rhizotomy alone or with L7-S3 ventral rhizotomy with and without total sympathectomy. The incidence of autonomous waves was < 15% 12 weeks after ventral or ventrodorsal rhizotomy, but acute sympathectomy at 13 weeks increased the incidence to 58% in these groups. With chronic sympathectomy the incidence was 100%. This suggests that the waves arise locally via a mechanism which is independent of L7-S3 dorsal roots, due to lack of a suppressive sympathetic pathway. Autonomous waves were inhibited by atropine after acute sympathectomy and by prazosin after chronic sympathectomy, but increased inhibition occurred after both drugs in either case. Adrenergic neuron depletion with 6-hydroxydopamine enhanced wave activity, which was incompletely inhibited by subsequent atropine. This implies that the peripheral reflex pathway has facilitatory alpha 1-adrenergic, muscarinic and also noncholinergic nonadrenergic elements. Clinically, sensory or sympathetic damage caused incontinence, but sympathectomy also caused high pressure waves, which may cause upper tract damage and treatment resistant incontinence in patients.