Overactive bladder (OAB) is a polyetiological nosology. Its symptoms are often characterized not only with detrusor hyperactivity, but also with the increased sensitivity of afferent fibers, which is clinically manifested as urgency. In addition, the disorders at the level of receptors expression and the synthesis of mediators lead to the development of bladder pain syndrome (BPS), which also significantly reduces the quality of life of patients. In recent years, the experimental animal studies achieved significant progress in understanding of the pathogenesis of lower urinary tract dysfunction. In particular, the broad understanding of the sensor properties of urothelium was obtained, which significantly increased the popularity of the urothelial theory of the development of idiopathic detrusor hyperactivity, as well as hypersensitivity and bladder pain. According to this theory, the pathological release of biologically active substance in the transitional epithelium in response to an extension of the bladder wall leads to clinical manifestations of the described conditions. In addition, due to the studies of the properties of receptors, ion channels, and mediators, the suggestion about the reduced efficiency of muscarinic receptor antagonists have been made in a large number of patients. Besides the acetylcholine control of the lower urinary tract, more and more attention is paid to other significant mechanisms of pathological conditions. The purpose of this part of the lecture is to systematize the available materials of basic research on the functioning of the lower urinary tract at the cellular level, as well as the mechanisms of action and questions of the effectiveness of pharmacological therapy for urinary disorders.
Keywords: clinical urology; neurophysiology of the lower urinary tract; overactive bladder; pathogenesis.