The present report concerns investigations of detrusor muscle adrenergic innervations in patients affected by bladder neuropathy secondary to diabetes without obstructive disturbances. Detrusor contractile activity evoked by NE is markedly reduced which can probably be attributed to receptor deficit. Urodynamic evaluation demonstrated a prevalence of sensory peripheral neuropathy than a motor conduction abnormality. In vitro study demonstrated that motor conduction abnormality of detrusor contractile activity is present early without bladder disturbances. Therefore early urodynamic measurements are necessary to evaluate bladder dysfunction and neuropathy in diabetic patients.