Benign prostatic enlargement is a common cause of bladder outlet obstruction. Recent work has demonstrated the important role played by the sympathetic nervous system in the control of prostatic muscle tone. Although isometric muscle strip studies and clinical trials have highlighted the influence of alpha-1 adrenoceptors, radioisotope ligand binding studies have demonstrated a relatively increased density of alpha-2 adrenoceptors in the muscle within prostatic tissue, the significance of which is as yet unexplained. Forty patients entered a study using pharmacological muscle strip experiments, radioligand binding assays and receptor autoradiography. Pharmacological data from these studies confirmed that contraction of prostatic muscle is mediated predominantly by alpha-1 adrenoceptor stimulation, with no evidence of significant alpha-2 adrenoceptor or cholinergic mediated effects. Radioligand binding studies confirmed that there is a higher concentration of alpha-1 binding sites as contrasted to alpha-2 within normal prostate, but that this relationship approaches equity in adenomatous prostate. Autoradiographic localisation demonstrated that alpha-1 adrenoceptor binding is predominant within prostatic stroma with only a small component of alpha-2 adrenoceptors in this compartment. This comprehensive study supports the suggestion that prostatic muscular contraction is controlled by the influence of the sympathetic nervous system acting via alpha-1 adrenoceptors. These findings support the therapeutic use of specific alpha-1 adrenoceptor blockade in the management of benign prostatic hyperplasia.

169 female patients with outlet obstruction have been studied urodynamically. The results of treatment of the outlet obstruction in 102 patients have been analysed and the reason for the failures discussed. Patients with stable detrusors and those with symptoms of recurrent urinary tract infection responded well to treatment, provided this relieved the obstruction adequately; symptomatic relief was less common in patients with unstable detrusors, despite adequate outflow readjustment.

Eighty patients with prostatic obstruction were entered into a double-blind parallel study of prazosin versus placebo. There were 25 withdrawals or exclusions, leaving 55 patients for analysis. Mean maximum flow rates increased significantly more in patients treated with prazosin than in those treated with placebo (P less than 0.005), but there was no significant reduction in maximum voiding pressure. The mean number of voids, recorded on diary cards, was reduced from an initial 10.0/24 h by 2.1 in the final week, a significantly greater reduction than in the placebo group (P less than 0.01). However, there were no statistically significant changes in the filling cystometrograms. When patients were classified as responders or non-responders in terms of bladder filling, urine flow, bladder emptying, weekly average of voids/24 h and nocturia, the proportion of patients responding to prazosin was significantly greater in all categories except bladder filling and emptying. It was concluded that prazosin at a dose of 2 mg bd is a safe and effective treatment for prostatic obstruction and may be used in patients awaiting surgery and those who are unfit for operation.

Doxazosin was well-tolerated and produced both urodynamic and symptomatic improvement in men with BPH, thereby providing a satisfactory alternative to existing drugs with the additional benefit of once daily dosage.