This dissertation provides the new data on the functioning of the transient receptor potential vanilloid 1 (TRPV1) ion channel in the urinary bladder tissues.This channel-receptor membrane protein, classically known as capsaicin (CAPS) receptor and thermosensor in peripheral nociceptors of mammals, in the last decade has been attractingthe increasing attention as a physiologically significant polymodal sensor of many physicochemical stimuli, i.e., burning temperatures (> 42 ° C), sour pH, mechanical stress, and a number of endogenous ligands including some signal lipids, spermine, oxytocin, and nitric oxide (NO). In this work, for the first time, it was demonstrated that TRPV1 is functionally present in the smooth muscle cells (SMCs) of the rat bladder detrusor. The application of CAPS increased the intracellular concentration of Ca2+ ([Ca2+]i) ions in 42% of isolated SMCs, and the spatial distribution of [Ca2 +]i indicates the localization of TRPV1 in the membranes of intracellular Ca2+ store, the endoplasmic reticulum. This conclusion was confirmed by the results of the electrophysiological recordings, in which CAPS was not able to trigger a classic, TRPV1-mediated membrane current (ITRPV1). Likewise,the fluorescence immunocytochemistry using anti-TRPV1 antibodies showed that this ion channel was localized intracellularly.The application of TRPV1 selective antagonists –capsazepine and BCTC –onto the strips of detrusor smooth muscle (DSM) blocked 20-40% of contraction caused by cholinomimeticcarbachol, indicating the participation of TRPV1 in the signaling cascade of cholinergic contraction of DSM. We also showed for the first time that NO donors can activate macroscopic ITRPV1 only in the presence of sulfhydryl-containing reagents (e.g., sodium nitroprusside) that accelerate the release of nitric oxide from donor molecules.In rats with streptozotocin-induced diabetes, the increase in the functional expression of TRPV1 in afferent neurons was observed. Still, the local effects of the CAPS onto DSM strips was found weakened. This indicates, on the one hand, the strengthening of the TRPV1-dependent afferent segment of the urination reflex arc during diabetes, and, on the other hand, the reduction of the contractile capacity of DSM in this pathology.
