The sympathetic innervation and adrenoreceptor function of the human lower urinary tract in the normal state and after parasympathetic denervation.

Adrenergic innervation of the human urinary bladder was studied in vitro in specimens excised during operation from six neurologically normal bladders and from five parasympathetically denervated (lower motor neuron lesion) bladders. Using a specific histochemical fluorescence technique, it was found that the adrenergic nerve terminals of the detrusor of the patients with lower motor neuron lesions were thicker, had a stronger fluorescence intensity, and were in most cases also more densely distributed than those of any of the six neurologically normal bladders examined. By recording the changes in the isometric tension of detrusor strips after different pharmacologic treatments, the existence of alpha-adrenergic receptors could be demonstrated in the parasympathetically denervated detrusor but not in the normal detrusor. The influence of alpha-adrenolytic treatment (phenoxybenzamine) was studied in vivo in seven patients with lower motor neuron lesions. In the cystometrograms, the bladders were more hypotonic and the "autonomous waves" appeared at a higher level of filling or were totally extinguished after this pharmacologic treatment. With an isotonic volume registration method, a bladder volume increase was recorded after alpha-adrenergic blockade. Using sphincterometry or urethral pressure profile studies, a decrease in the urethral resistance was observed after alpha-adrenolytic treatment.