Six spinal cord injured patients were evaluated with cystometry, bladder electromyography, and external urethal spincter pressure profiles before and after propranolol hydrochloride administration. Bladder contractility was significantly augmented, and therefore was associated with decreased beta-sympathetic bladder stimulation. The results of these clinical neurophysiological investigations suggest inhibitory influences upon the smooth muscle of the human urinary bladder via beta-sympathetic receptors.