The therapy of symptoms of the lower urinary tract that in most cases are caused by benign prostatic hyperplasia is one of challenges for modern medicine. Knowing the origin of bladder muscle hyperactivity will promote the treatment in this group of patients. The studies of interstitial cells of Cajal in the urinary bladder open up new opportunities to widen our understanding of bladder physiology. The purpose of this study is to conduct an analytical review of the literature on the role of interstitial cells of Cajal in the physiology of the urinary bladder. We investigated the current literature highlighting the morphological and physiological significance of interstitial cells of Cajal in the urinary bladder. Interstitial cells of Cajal are in close proximity to muscle cells, vegetative nerve endings and urothelial cells. There is increasing evidence that interstitial cells of Cajal play a role in the development of lower urinary tract symptoms. Interstitial cells of Cajal may be responsible for generating electrical potentials and inducing detrusor muscle contractions. New pathomechanisms of the development of bladder hyperactivity were put forward, namely: impairment of spontaneous contractility caused by altered signal transduction of interstitial Cajal cells between nerves and detrusor muscle cells; change in signal transmission through suburothelial interstitial cells of Cajal. The c–kit receptor is not only a marker for identifying these cells, but may also play a critical role in controlling bladder function. Interstitial cells of Cajal, discovered more than 100 years ago, are still remaining a poorly studied object. Having long processes, interstitial cells of Cajal form multiple contacts with smooth muscle and nerve cells, building up a specific network. Current knowledge about interstitial cells of Cajal in the urinary bladder suggest that these cells and c–kit receptors may become a new “target” for the pharmaceutical therapy of lower urinary tract symptoms and overactive bladder.

We conducted an analytical review of the literature on the problem of bladder decompensation in patients with benign prostatic hyperplasia. Benign prostatic hyperplasia is one of the most common diseases in aging men. As is known, with the development of benign prostatic hyperplasia due to infravesicular obstruction, the resistance to urine flow increases. As a result of a prolonged overload, the bladder is restructured, and it goes through three successive stages: compensation, subcompensation, and decompensation. Irreversible changes develop in the epithelial, muscular, and nerve tissues of the bladder. With benign prostatic hyperplasia due to intravesical hypertension, persistent microcirculation disorders occur in the walls of the bladder, which leads to the appearance of chronic detrusor ischemia, and can be a predictor of its fibrotic changes and decompensation. There is a correlation between the pathology of the vascular system and the development of symptoms of the lower urinary tract against the background of benign prostatic hyperplasia. Improvement of lower urinary tract perfusion can be considered a therapeutic strategy for the treatment of bladder dysfunction.