Kallikrein-kinin system pathogenetic importance in experimental benign prostatic hyperplasia

Aim: To analyze the mechanisms of regulation of the body's proteolytic systems during inflammation, detection of inflammation markers in blood and prostate secretions in the experimental benign prostatic hyperplasia in rats.

Materials and Methods: The study was conducted on 30 male rats on the model of benign prostatic hyperplasia. Rats were randomized as following: the 1st group (n=6) - intact animals; the 2nd group (n=24) - rats with benign prostatic hyperplasia.

Results: The prostate gland inflammatory damage was also evidenced by the prostate secretion proteolytic potential increase in 9 times as the result of kallikrein activity enhancement on the 21st day of the trial which leads to massive kininogenesis. The analogous kallikrein activity increase (in 3,2 times) we registered in blood serum. An acute kallikrein activity increase in case of benign prostatic hyperplasia is probably compensated by an increase in the activity of its specific inhibitor - α2-macroglobulin, the level of which in conditions of investigated pathology increased in 3,25 times on the 21st day of the trial compared to intact rats, and by the proteolytic potential increase resulted in the inhibitory activity of alpha1 proteinase inhibitor content increase in 2,25 times (a protein of the acute stage of inflammation).

Conclusions: An increase in the content and activity of kallikrein-kinin system components in the prostate secretion testifies to its inflammatory damage and the disturbance of the hematoprostatic barrier permeability which can be an important diagnostic criterion.