Серед спонтанно активних іонних каналів внутрішньої ядерної мембраникардіоміоцитів, найчастіше реєстрували струм через LCC-канали з провідністю 209 ± 13 пСм. Ці канали характеризуються потенціалзалежністю, вибірковоюпроникністю одновалентних катіонів К+та Na+і непроникністю Clта Са2+.Послідовність ефективності інгібування LCC-каналів ядерної мембраникардіоміоцитів агоністами та інгібіторами н-холінорецепторів і зміїними токсинамивиглядає так: DhβE > d-тубокурарин ≈ нікотин > NT II > dFBr > дитилін ≈атракуріум ≈ піпекуронію бромід > рокуронію бромід > α-CTX. Не впливають надосліджувані канали: гексаметоній, α-конотоксин PeIA, MLA, PNU 282987 ікарбахолін.Ро IP3-рецепторів внутрішньої ядерної мембрани кардіоміоцитів єпотенціалзалежною, зростає зі збільшенням концентрації ІР3 (максимум за10 мкмоль/л ІР3 у середовищі). IP3-рецептори також характеризуються різноючутливістю до Са2+: для частини притаманна класична дзвоноподібна залежність відйого концентрації (з повним інгібуванням за 1 мкмоль/л Са2+), тоді як для іншоїчастини графік залежності Ро від концентрації Са2+ зміщений праворуч й інгібуванняпочинається за 10 мкмоль/л Са2+.Отже, у ядерній мембрані кардіоміоцитів наявні два підтипи ІР3-рецепторів,котрі відрізняються за чутливістю Са2+ та LCC-канали, котрі з різною ефективністюінгібуються агоністами й інгібіторами н-холінорецепторів.^UFor the first time, several types of spontaneously active channels with differentconductance (from 10–340 pS) have been detected in the inner nuclear membrane ofcardiomyocytes. Among them, LCC-channels with conductance 209 ± 13 pS are the mostexpressed. These channels have relatively slow kinetics; at positive potentials (+40 mV)they remain in the open state most of the time (NPо = 3.11), whereas at negative potentials(-40 mV) their activity decreases (NPо = 0.72). K+ions permeate well through LCCchannels, to a lesser extent Na+, and LCC-channels are impermeable to Cland divalentCa2+ cations. Relatively high density combined with high conductance of LCC-channels inthe nuclear membrane indicates their important physiological role in regulating nuclearfunctions.Purified neurotoxin II at a concentration of 25 μM reduces amplitude of the currentthrough these channels by 13 %. After applying 1–2 mM of α-cobratoxin, a slight channelflickering is observed. The effects of all tested substances are reversed – after washingwith the working solution, current through the LCC-channels returns to the control values.Under the influence of d-tubocurarine (200 μM), the amplitude of the currentthrough the nuclear membrane's LCC-channels in cardiomyocytes decreases by 45 %.Under the influence of 25 μM DhβE, a 40 % decrease in current through the channel isobserved. At high concentrations of atracurium and dithylinum, Po decreases and channelflickering is observed, indicating physical blockade of the channel pore in its open state.However, there is no complete blocking even at 2 mM blocker concentration. Nondepolarizing neuromuscular relaxant rocuronium bromide dose-dependently reducescurrent amplitude through the channels, inhibits them by half at concentration of 2 mMand reduces probability of them being in an open state by half.A similar effect on LCC-channels functional activity is induced by pipecuroniumbromide. Other investigated n-cholinoinhibitors – hexamethonium, MLA, α-conotoxinPeIA were proved ineffective. In the following series of experiments, the effects of ncholinoreceptor agonists are tested. In particular, nicotine at a concentration of 10 to 200μM dose-dependently decreases current amplitude through LCC-channels. After dFBr 23application at a concentration of 200 μM, the amplitude of the current through the channeldecreases by 21 % and channel flickering is observed. Whereas, other investigated ncholinoreceptor agonists – PNU 282987 and carbachol did not cause statisticallysignificant changes in LCC-channels functioning.The most effective among tested n-cholinoreceptor agonists and inhibitors and alsosnake toxins are: DhβE > d-tubocurarine ≈ nicotine > NT II > dFBr > dithylinum ≈atacurium ≈ pipecuronium bromide > rocuronium bromide > α-CTX.In the nuclear membrane of cardiomyocytes, a channel that is activated by IP3 (0.2–20 μM) and inhibited by 2-APB (50 μM) was detected. On this basis, we concluded thatthe channel is IP3Rs. It's known from the literature that the most expressed IP3Rs incardiomyocytes are type II and we have confirmed that via immunohistochemical analysis.Probability of IP3Rs being in open state (Po) is potential-dependent, with higher activity ofIP3Rs observed at positive potential values (+40 mV Po = 0.043, +60 mV Ро = 0.125),while at negative values their activity decreases (-40 mV Ро = 0.025, -60 mV Ро = 0.005).The probability of an open state of investigated receptors increases with increasing IP3concentration and peaks at a concentration of 10 μM IP3 in the solution (NPo = 0.292). Inthe following series of experiments, we investigate the effect of Ca2+ ions in differentconcentrations on IP3Rs activity. In particular, we were able to detect two subtypes ofIP3Rs, one of which is inhibited by high concentrations of Ca2+, which corresponds to theclassical pattern of bell-shaped activity dependent on Ca2+ concentration. This is alsoconfirmed by literature, according to which high Ca2+ concentrations inactivate purifiedcardiac IP3Rs. The other type of IP3Rs has a significantly right-shifted activitydependence, their inhibition starts at 10 μM Ca2+, but a few single-channel openingsremain at 1 mM of Ca2+ in the solution.The properties of IP3Rs in the nuclear membrane of cardiomyocytes differ sharplyfrom both neuronal IP3Rs type I receptors and heterologously expressed IP3Rs type II.This may be explained by the influence of post-translational modifications and themolecular environment. Such heterogeneity contributes significantly to temporal andspatial propagation of the intracellular calcium signal in the nucleus.The results demonstrate two subtypes of IP3 receptors in the nuclear membrane ofcardiomyocytes that differ in sensitivity to IP3, Ca2+ and LCC-channels, which areinhibited by agonists and inhibitors of n-cholinoreceptors with different effectiveness.