Alfuzosin Hydrochloride for the Treatment of Benign Prostatic Hyperplasia

Mary Lee


Am J Health Syst Pharm. 2003;60(14) 

In This Article

Prostate Physiology and the Role of

A normal prostate gland comprises smooth muscle or stromal tissue and glandular tissue. The prostate produces some secretions that are included in the male ejaculate, and another secretion that may exert an antibacterial effect. Unlike a normal prostate, the prostate in patients with BPH contains a higher ratio of stromal to glandular tissue (5:1).[4] The smooth muscle is innervated by α-adrenergic receptor stimulation α1 and α2. The outer prostatic capsule (outer shell), bladder neck (base), and proximal urethra also have a high concentration of α1-adrenergic receptors. Excessive stimulation of postsynaptic α1-adrenergic receptor stimulation causes the smooth muscle of the prostate, prostatic capsule, bladder neck, and proximal urethra to contract, resulting in a decrease in the urethral lumen and obstructive voiding symptoms. This causes difficulty in urination, a decreased force of urinary stream, urinary hesitancy, straining to void, incomplete bladder emptying, urinary dribbling, and an intermittent urinary stream. Stimulation of presynaptic α2-adrenergic receptors has an unknown effect on the prostate.[5]

Alpha adrenergic receptors exist in many other extraprostatic tissues. Stimulation of α1-receptors in vascular smooth muscle can result in muscle contraction and elevated blood pressure. Conversely, inhibition of α1-adrenergic receptors can cause hypotension, syncope, and dizziness. Stimulation of α2-adrenergic receptors inhibits presynaptic catecholamine release. In contrast, inhibition of α2-adrenergic receptors increases catecholamine release, resulting in enhanced cardiac conduction and automaticity. Thus, α1-adrenergic antagonists aid in reducing the symptoms of BPH, but the lack of selectivity for α1-adrenergic receptors in the prostate can produce adverse cardiovascular effects.

Studies have identified several subtypes of α1-adrenergic receptors in the prostate. Approximately 70% of all α1-adrenergic receptors in the prostate are of the subtype α1A; the rest are subtype α1B or α1D.[6,7] All α1-adrenergic antagonists inhibit all subtypes of the α1-receptors in the prostate to some extent.[8]


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