T he search for nonhormonal pharmacological agents capable of reducing out flow obstruction caused by benign prostatic hyperplasia (BPH) began in the 1970s when alpha adrenergic receptors were demonstrated within the smooth
muscle element of prostatic adenomas, the prostatic capsule, and the bladder neck.
Recently, many studies have confirmed that the alpha adrenoceptor blockade sub-
jectively and objectively reduces symptoms and urodynamic parameters in bladder
outflow obstruction. Very longterm effects of the alpha blockade upon the pro-state are not yet known. There is no direct evidence of a decrease in the stromal smooth muscle bulk or in the total prostate volume after longterm treatment with alpha adrenoceptor blockers in man. The endocrinebased therapies, such as stilbestrol, luteinizing hormonereleasing hormone analogues, antiandrogens flutamide, and cyproterone acetate, have sometimes been used to treat BPH, but with a limited efficacy and prominent sideeffects such as loss of libido, impotence, hot flushes, and gynecomastia. Although it has been shown that some of these therapies may shrink the prostate, the sideeffects are intolerable to most patient. On the other hand, new 5 alpha reductaseinhibiting agents are able to block the effects of androgen within the prostate without a systemic antiandrogen activity. Since the effects of androgens are particularly directed at the glandular element of the prostate rather than at the smooth muscle, the combined use of alphaadrenoceptor blockers and 5 alphareductase inhibitors could theoretically produce an additive effect in the treatment of BPH. The indications of medical treatment for BPH include patients with mild to moderate symptoms, especially if they are reluctant to undergo surgery, and those who are not medically eligible to surgery.
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