Tamsulosin selectively and competitively blocks postsynaptic alpha-1 adrenergic receptors located in the smooth muscle of the prostate, bladder neck and prostatic urethra , and alpha-1-adrenergic receptors, mainly located in the body of the bladder define equipoise. This leads to a reduction in smooth muscle tone of the prostate, bladder neck and prostatic urethra and detrusor improve function. This reduces the symptoms of obstruction and irritation associated with benign prostatic hyperplasia. Typically, the therapeutic effect is at 2 weeks after the beginning of reception of the preparation, although some patients, a decrease in symptoms observed after the first dose. Tamsulosin ability to influence the alpha-1A adrenoceptors 20 times greater than its ability to interact with alpha-1 adrenoceptors located in vascular smooth muscle. Due to such a high selectivity of the drug does not cause any clinically significant reduction in systemic blood pressure in both hypertensive patients and in patients with normal baseline .
Finasteride – a synthetic 4-azasteroid, a specific inhibitor of the intracellular enzyme 5-alpha-reductase type II. Last converts testosterone into the more active androgen – 5-alpha-dihydrotestosterone .The normal function and growth of the prostate gland, including its hypertrophied tissue is dependent on the conversion of testosterone to define equipoise. Finasteride has no effect on the androgenic receptors. In healthy volunteers, proliferation and apoptosis of prostate cells are balanced due to the interaction of factors that inhibit and stimulate growth. Although the etiological factors, on a molecular level causing prostatic hyperplasia are not yet known, probable that in this process plays a role. Specific inhibitors of type II 5-alpha-reductase reduce the concentration in the prostate and promote regression of prostate hyperplasia. According to clinical studies, treatment with finasteride rapidly reduces the concentration in the plasma by 70%, resulting in a decrease in prostate volume. At constant reception statistically significant effects recorded after 3 months (decrease prostate volume by about 20%) and 7 months (decrease in severity of symptoms associated with benign prostatic hyperplasia).
In humans, there are two kinds of 5-alpha reductase inhibitor: I and P. Their distribution in tissues differently: in prostate, testis and epididymis, glans penis, scrotum, seminal vesicle, liver, and the chest occurs type II isozyme; Type I is found mainly in the skin of the head, back and chest, sebaceous glands, in the liver, kidney and adrenal glands. Finasteride inhibits primarily type II isozyme, is responsible for most of the in the blood. A single dose of finasteride quickly and significantly change the concentration of define equipoise in plasma. A single dose of 5 mg of finasteride reducing DHT concentration in plasma is 75%, which is 24 o’clock reaches its minimum, and then returns to its original level within 7 days.
Repeated reception finasteride is effective. Finasteride decreases the concentration in the prostate itself to <15% and provides a corresponding increase in testosterone in the prostate. Compared with surgical or chemical castration, treatment with finasteride is accompanied by a significantly greater decrease in the level in the prostate. Prostate-specific antigen – a sensitive and specific marker of prostate carcinoma androgenozavisimy. In most cases, after a few months of treatment with finasteride, a rapid decrease in levels, and then setting it to low values. After 1 year receiving finasteride 5 mg average concentration is reduced by 50%.
Finasteride does not exhibit affinity for androgen receptors and has no other hormonal action. Following the discovery of the 5-alpha-reductase deficiency syndrome and the description of the 5-alpha-reductase type II (male hermaphroditism type) the role of androgens in benign prostatic hyperplasia was again revised.
Prostate development is dependent ondefine equipoise strong androgen. When failure of 5-alpha-reductase in the background of normal or high testosterone levels in adulthood there is atrophy of the prostate. Activates the androgen receptor to form after the accession to the dimers, which are entering into a relationship with directly or indirectly, contribute to cell proliferation by changing the expression of genes responsible for proliferation and apoptosis. In the intact prostate apoptosis and proliferation processes are in equilibrium. Despite the fact that the factors that trigger prostate hyperplasia at the molecular level, are not known, the role of the is very likely. Specific inhibitors of 5-alpha-reductase type II can reduce the concentration define equipoisein the prostate and promote regression of hyperplastic prostate.