Renin-angiotensin and kallikrein-kinin systems: a significance in the benign prostatic hyperplasia pathogenesis

Abstract

Background . Benign prostatic hyperplasia (BPH) is the most common disease in older men. BPH pathophysiology is poorly understood. Although, it is known that the transmission of androgenergic signals and the reactivity of prostate's stroma as well as inflammatory factors are known to be the main pathophysiological mechanisms. In this regard, it is of interest to study the activity of enzymes and their inhibitors of the renin-angiotensin and kallikrein-kinin systems in BPH. Objectives. The study of new molecular mechanisms of the BPH pathogenesis. Materials and methods. The activity of the angiotensin-converting enzyme (ACE), the kallikrein-like activity and the prekallikrein content were determined. The total arginine-esterase activity was the inhibitory activity of the a1-proteinase inhibitor and a2-macroglobulin in the prostate secretion in men with BPH. A sharp increase of ACE activity in BPH leads to the accumulation of angiotensin II in the prostate secretion. A consequence of the activation of ACE in prostate secretion is a decrease in the content of bradykinin. An increase of the a1-proteinase inhibitor suppressing activity in prostate secretion at BPH indicates an increase in leukocyte degranulation activity during the development of the inflammatory process. Results. A sharp increase of ACE activity in BPH leads to the accumulation of angiotensin II in the prostate secretion. A consequence of the activation of ACE in prostate secretion is a decrease in the content of bradykinin. An increase of the a1-proteinase inhibitor suppressing activity in prostate secretion at BPH indicates an increase in leukocyte degranulation activity during the development of the inflammatory process. Conclusion. Metabolic basis for the BPH development can be mediated by impaired metathesis of angiotensin II and bradykinin in the prostate.