The symptoms of BPH (e.g., urethral obstruction leading to weak stream, urinary frequency, and nocturia) result from mechanical pressure on the urethra (due to an increase in smooth muscle mass) and an a-mediated increase in smooth muscle tone in the prostate and neck of the bladder. a1 receptors in the trigone muscle of the bladder and urethra contribute to the resistance to outflow of urine; prazosin reduces this. The efficacy and importance of a receptor antagonists in the medical treatment of BPH have been demonstrated in multiple controlled clinical trials. Finasteride (propecia) and dutasteride (avodart), which inhibit conversion of testosterone to dihy-drotestosterone (see Chapter 58), can reduce prostate volume in some patients; however, their overall efficacy appears less than that of a1 receptor antagonists. Selective a1 receptor antagonists have efficacy in BPH owing to relaxation of smooth muscle in the bladder neck, prostate capsule, and prostatic urethra. Recent studies show that combination therapy with doxazosin and finasteride reduces the risk of overall clinical progression of BPH significantly more than treatment with either drug alone. Prazosin, terazosin, doxazosin, tamsulosin, and alfuzosin have been studied extensively and used widely in patients with BPH. With the exception of tamsulosin, the comparative efficacies of each of these drugs appear similar. Tamsulosin at the recommended dose of 0.4 mg daily is less likely to cause orthostatic hypotension than are the other drugs. The predominant a1 receptor subtype in the human prostate appears to be a1A.
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