ATC Group: G04C Drugs used in benign prostatic hypertrophy

Alfuzosin is an orally active quinazoline derivative. It is a selective, peripherally acting antagonist of postsynaptic alpha-1-adrenoceptors. In vitro pharmacological studies have documented the selectivity of alfuzosin for the alpha-1-adrenoreceptors located in the prostate, bladder base and prostatic urethra.

Dutasteride reduces circulating levels of dihydrotestosterone (DHT) by inhibiting both type 1 and type 2, 5α-reductase isoenzymes which are responsible for the conversion of testosterone to DHT.

Finasteride is a competitive inhibitor of human 5α-reductase, an intracellular enzyme which metabolises testosterone into the more potent androgen, dihydrotestosterone (DHT). In benign prostatic hyperplasia (BPH), enlargement of the prostate gland is dependent upon the conversion of testosterone to DHT within the prostate. Finasteride is highly effective in reducing circulating and intraprostatic DHT. Finasteride has no affinity for the androgen receptor.

Silodosin is highly selective for α_1A-adrenoreceptors that are primarily located in the human prostate, bladder base, bladder neck, prostatic capsule and prostatic urethra. Blockade of these α_1A-adrenoreceptors causes smooth muscle in these tissues to relax, thus decreasing bladder outlet resistance, without affecting detrusor smooth muscle contractility.

Tamsulosin binds selectively and competitively to post-synaptic α₁-adrenoreceptors, prevailingly their subtypes designated α_1A and α_1D. Thus relaxation of smooth muscles of the prostate and urethra is achieved, which leads to a reduction of tonus and an improvement of the urinary flow.

Although the exact mechanism of the hypotensive action is not established, the relaxation of peripheral blood vessels appears to be produced mainly by competitive antagonism of post-synaptic alpha-adrenoceptors. Terazosin usually produces an initial gradual decrease in blood pressure followed by a sustained antihypertensive action.