Summary. The adrenergic and cholinergic innervation of the bladder was studied in streptozotocin-diabetic rats. The presence of hypertrophy and distension in the 'diabetic' bladders necessitates care in assessing changes occurring in the nerves, factors which are also relevant to clinical histochemical studies. Biochemical assays of cholinergic enzymes revealed decreased activities per g wet weight tissue. However, the total activities of choline acetyltransferase and acetylcholinesterase per whole bladder were significantly increased after 2 weeks of diabetes with greater changes by 8 weeks. Total dopamine levels per bladder were significantly higher than in control rats in the 2-week but not the 8-week group of animals; this may indicate an initial increase in adrenergic nerve activity. There was no impairment in the ability of the detrusor muscle to respond to noradrenaline, acetylcholine or to cholinergic nerve stimulation. Shortly after induction of diabetes streptozotocin-treated rats display polyuria. It is proposed that the activity of the bladder is therefore stimulated to allow greater volumes of urine to be passed. The results are discussed in relation to human diabetes mellitus where clinical studies have implicated a neuropathic origin to bladder dysfunction.Key words: Bladder, diabetic rats, adrenergic nerves, cholinergic nerves, polyuria, neuropathy.Clinical studies on bladder function in patients suffering from diabetes mellitus have reported that an early indication of dysfunction is increased bladder capacity and size, the incidence of such abnormalities has been reported as being as high as 87% in a group of juvenileonset diabetic patients [21]. Later stages are associated with atony of the bladder and urinary retention [16,21,29], and recent literature reveals that the clinical treatment of these symptoms is still under discussion [19,32, 39]. Several studies have correlated the presence of abnormalities in the bladder with signs of peripheral neuropathy [4,5,17]. In addition, clinical investigations of bladder innervation and function have led to the conclusion that bladder dysfunction is a manifestation of autonomic neuropathy in diabetes mellitus [3,7,15,20]. In particular, a defect in the sensory nerves of the bladder has been implicated as the cause of bladder distension in diabetic patients, whilst incomplete bladder emptying occurs as a result of impaired detrusor activity [5,6,16,36]. Histochemical studies on diabetic patients [20] and the diabetic Chinese hamster [10] have revealed reduced staining for acetylcholinesterase in the 'diabetic' bladder, and consequently it has been suggested that an alteration in the cholinergic innervation of the bladder may be one factor involved in bladder dysfunction.In the present investigation, bladder dysfunction was studied in the early stages of streptozotocininduced diabetes in rats, an animal model of juvenileonset diabetes. Distension and hypertrophy of the bladder occurred rapidly after the onset of diabetes, and the adrenergic and choliner...