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1.
A mathematical model for the excitation-contraction coupling within a functional unit (locus) of the small bowel is proposed. The model assumes that: the functional unit is an electromyogenic syncytium; its electrical activity is defined by kinetics of L- and T-type Ca2+-channels, mixed Ca2+-dependent K+-channels, potential-sensitive K+-channels and Cl–-channels; the basic neural circuit, represented by the cholinergic and adrenergic neurones, provides a regulatory input to the functional unit via receptor-linked L-type Ca2+-channels; the smooth muscle syncytium of the locus is a null-dimensional contractile system. With the proposed model the dynamics of active force generation is determined entirely by the concentration of cytosolic calcium. The model describes electrical processes of the propagation of excitation along the neural circuit, chemical mechanisms of nerve-pulse transmission at the synaptic zones and the dynamics of active force generation. Numerical simulations have shown that it is capable of displaying different electrical patterns and mechanical responses of the locus. The simulated effects of: tetrodotoxin, -bungarotoxin, salts of divalent cations, inhibitors of catechol-O-methyltransferase and neuronal uptake mechanisms, and changes in the concentration of external Ca2+ on the dynamics of force generation have been analysed. The results are in good qualitative and quantitative agreement with results of experiments conducted on the visceral smooth muscle of the small bowel. 相似文献
2.
Juliane Brun Katrin A. Lutz Katharina M. H. Neumayer Gerd Klein Tanja Seeger Tatiana Uynuk-Ool Katharina W?rg?tter Sandra Schmid Udo Kraushaar Elke Guenther Bernd Rolauffs Wilhelm K. Aicher Melanie L. Hart 《PloS one》2015,10(12)
The use of mesenchymal stromal cells (MSCs) differentiated toward a smooth muscle cell (SMC) phenotype may provide an alternative for investigators interested in regenerating urinary tract organs such as the bladder where autologous smooth muscle cells cannot be used or are unavailable. In this study we measured the effects of good manufacturing practice (GMP)-compliant expansion followed by myogenic differentiation of human MSCs on the expression of a range of contractile (from early to late) myogenic markers in relation to the electrophysiological parameters to assess the functional role of the differentiated MSCs and found that differentiation of MSCs associated with electrophysiological competence comparable to bladder SMCs. Within 1–2 weeks of myogenic differentiation, differentiating MSCs significantly expressed alpha smooth muscle actin (αSMA; ACTA2), transgelin (TAGLN), calponin (CNN1), and smooth muscle myosin heavy chain (SM-MHC; MYH11) according to qRT-PCR and/or immunofluorescence and Western blot. Voltage-gated Na+ current levels also increased within the same time period following myogenic differentiation. In contrast to undifferentiated MSCs, differentiated MSCs and bladder SMCs exhibited elevated cytosolic Ca2+ transients in response to K+-induced depolarization and contracted in response to K+ indicating functional maturation of differentiated MSCs. Depolarization was suppressed by Cd2+, an inhibitor of voltage-gated Ca2+-channels. The expression of Na+-channels was pharmacologically identified as the Nav1.4 subtype, while the K+ and Ca2+ ion channels were identified by gene expression of KCNMA1, CACNA1C and CACNA1H which encode for the large conductance Ca2+-activated K+ channel BKCa channels, Cav1.2 L-type Ca2+ channels and Cav3.2 T-type Ca2+ channels, respectively. This protocol may be used to differentiate adult MSCs into smooth muscle-like cells with an intermediate-to-late SMC contractile phenotype exhibiting voltage-gated ion channel activity comparable to bladder SMCs which may be important for urological regenerative medicine applications. 相似文献
3.
Patrik Rorsman Lena Eliasson Takahiro Kanno Quan Zhang Sven Gopel 《Progress in biophysics and molecular biology》2011,107(2):224-235
When exposed to intermediate glucose concentrations (6–16 mol/l), pancreatic β-cells in intact islets generate bursts of action potentials (superimposed on depolarised plateaux) separated by repolarised electrically silent intervals. First described more than 40 years ago, these oscillations have continued to intrigue β-cell electrophysiologists. To date, most studies of β-cell ion channels have been performed on isolated cells maintained in tissue culture (that do not burst). Here we will review the electrophysiological properties of β-cells in intact, freshly isolated, mouse pancreatic islets. We will consider the role of ATP-regulated K+-channels (KATP-channels), small-conductance Ca2+-activated K+-channels and voltage-gated Ca2+-channels in the generation of the bursts. Our data indicate that KATP-channels not only constitute the glucose-regulated resting conductance in the β-cell but also provide a variable K+-conductance that influence the duration of the bursts of action potentials and the silent intervals. We show that inactivation of the voltage-gated Ca2+-current is negligible at voltages corresponding to the plateau potential and consequently unlikely to play a major role in the termination of the burst. Finally, we propose a model for glucose-induced β-cell electrical activity based on observations made in intact pancreatic islets. 相似文献
4.
《Molecular membrane biology》2013,30(2):83-110
Freshly dissociated cells from the stomach muscularis of the toad Bufo marinus have been employed to carry out a systematic set of electrophysiological studies on the membrane properties of smooth muscle. The existence of Ca2+-activated K+ channels became apparent during the first studies under current clamp. In subsequent studies under voltage clamp, a Ca2+-activated, TEA-sensitive outward current was evident, and it was more than an order of magnitude larger than any other current observed in the cells. The channel responsible, at least in part, for this large outward current has been identified on the basis of single-channel records, and some of its main characteristics have been studied. It is similar in many respects to the large-conductance, Ca2+-activated K+ channel seen in other preparations. This channel has now been found in a considerable diversity of smooth muscle types. 相似文献
5.
Anatoly Soloviev Sergey Tishkin Irina Ivanova Sergey Zelensky Victor Dosenko Sergey Kyrychenko Robert S. Moreland 《Life sciences》2009,84(5-6):164-171
AimsThe goal of this study was to evaluate the influence of γ-irradiation on Ca2+-activated K+ channel (BKCa) function and expression in rat thoracic aorta.Main methodsAortic cells or tissues were studied by the measurement of force versus [Ca2+]i, patch-clamp technique, and RT-PCR.Key findingsStimulation of smooth muscle cells with depolarizing voltage steps showed expression of outward K+ currents. Paxilline, an inhibitor of BKCa channels, decreased outward K+ current density. Outward currents in smooth muscle cells obtained from irradiated animals 9 and 30 days following radiation exposure demonstrated a significant decrease in K+ current density. Paxilline decreased K+ current in cells obtained 9 days, but was without effect 30 days after irradiation suggesting the absence of BKCa channels. Aortic tissue from irradiated animals showed progressively enhanced contractile responses to phenylephrine in the post-irradiation period of 9 and 30 days. The concomitant Ca2+ transients were significantly smaller, as compared to tissues from control animals, 9 days following irradiation but were increased above control levels 30 days following irradiation. Irradiation produced a decrease in BKCa α- and β1-subunit mRNA levels in aortic smooth muscle cells suggesting that the vasorelaxant effect of these channels may be diminished.SignificanceThese results suggest that the enhanced contractility of vascular tissue from animals exposed to radiation may result from an increase in myofilament Ca2+ sensitivity in the early post-irradiation period and a decrease in BKCa channel expression in the late post-irradiation period. 相似文献
6.
The existence of [Ca2+]i-activated K+-channels in the pancreatic β-cell membrane is based in two observations: quinine inhibits K+-permeability and, increasing intracellular Ca2+ stimulates it. The changes in K+-permeability of the β-cell have been monitored electrically by combining measurements of the dependence of the membrane potential on external K+ concentration and input resistance. The changes in the passive 42K and 86Rb efflux from the whole islet have been measured directly. Intracellular Ca2+ has been increased by various means, including increasing extracellular Ca2+, addition of the Ca2+-ionophore A23187 or noradrenaline and application of mitochondrial uncouplers and blockers. In addition to quinine, many other substances have been found to inhibit or modulate the [Ca2+]i-activated K+-channel. The most important of these is the natural stimulus for insulin secretion, glucose. Glucose may inhibit K+-permeability by lowering intracellular Ca2+. Glibenclamide, a hypoglycaemic sulphonylurea, is about 25 times more active than quinine in blocking the K+-channel in β-cells. The methylxanthines, c-AMP, various calmodulin inhibitors and Ba2+ also inhibit K+-permeability. Genetically diabetic mice have been studied and show an alteration in the [Ca2+]i-activated K+-channel.It is concluded that the [Ca2+]i-activated K+-channel plays a major role in the normal function of the pancreatic β-cell. The study of its properties should prove valuable for the understanding and treatment of diabetes. 相似文献
7.
《Journal of insect physiology》1986,32(3):239-248
The myotropic neuropeptide proctolin is, in additional to its action on proctodaeum and on some other systems, highly effective on the hyperneural muscle of Periplaneta americana and evokes long-term contractions. During this proctolin response the input resistance (Rinput) increases by about 25% accompanied by only slight depolarization. These processes require extracellular Ca2+ but are still present in Na+-free solution.Junction potentials evoked by threshold stimulation of the nerve are not affected by proctolin. Synaptic processes do not seem to be important for the proctolin action on hyperneural muscle. It is more likely that the whole membrane of the muscle fibre serves as target for proctolin. Proctolin reduces the threshold for neurally evoked muscle contractions, the only available route of excitation since the muscle fibres themselves are not electrically excitable.The K+-channel blocker 4-aminopyridine may evoke contraction as well as proctolin, but this is only a transitory response. In contrast to proctolin, 4-aminopyridine is still effective after blocking the Ca2+-channels by Co2+, but the response is smaller. Therefore proctolin seems to be primarily effective via Ca2+-channels, whereas 4-aminopyridine exerts its effects via K+-channels. The decrease in membrane conductance produced by proctolin could result from a Ca2+-dependent reduction of the K+-outward current. 相似文献
8.
Maria Grazia Zizzo Alessandra Bonomo Natale Belluardo Flavia Mulè Rosa Serio 《Life sciences》2009,84(21-22):772-778
AimsWe investigated the effects induced by exogenous adenosine on the spontaneous contractile activity of the longitudinal muscle of a mouse ileum, the receptor subtypes activated, the involvement of enteric nerves and whether opening of K+ channels was a downstream event leading to the observed effects.Main methodsMechanical responses of the mouse ileal longitudinal muscle to adenosine were examined in vitro as changes in isometric tension.Key findingsAdenosine caused a concentration-dependent reduction of the spontaneous contraction amplitude of the ileal longitudinal muscle up to its complete disappearance. This effect induced was markedly reduced by an A1 receptor antagonist, but not by A2 and A3 receptor antagonists and mimicked only by the A1 receptor agonist. Adenosine uptake inhibitors did not change adenosine potency. A1 receptor expression was detected at the smooth muscle level. Adenosine responses were insensitive to tetrodotoxin, atropine or nitric oxide synthase inhibitor. Tetraethylammonium and iberiotoxin, BKCa channel blockers, significantly reduced adenosine effects, whilst 4-aminopyridine, a Kv blocker, apamin, a small conductance Ca2+-activated K+ (SKCa) channel blocker, charybdotoxin, an intermediate conductance Ca2+-activated K+ (IKCa) and BKCa channel blocker, or glibenclamide, an ATP-sensitive K+ channel blocker, had no effects. The combination of apamin plus iberiotoxin caused a reduction of the purinergic effects greater than iberiotoxin alone.SignificanceAdenosine acts as an inhibitory modulator of the contractility of mouse ileal longitudinal muscle through postjunctional A1 receptors, which in turn would induce opening of BKCa and SKCa potassium channels. This study would provide new insight in the pharmacology of purinergic receptors involved in the modulation of the gastrointestinal contractility. 相似文献
9.
Priyanka Verma Aparna K Sharma Hari Shankar Alpana Sharma D. N. Rao 《Biological trace element research》2018,183(2):325-334
Cadmium is an environmental pollutant closely linked with cardiovascular diseases that seems to involve endothelium dysfunction and reduced nitric oxide (NO) bioavailability. Knowing that NO causes dilatation through the activation of potassium channels and Na+/K+-ATPase, we aimed to determine whether acute cadmium administration (10 μM) alters the participation of K+ channels, voltage-activated calcium channel, and Na+/K+-ATPase activity in vascular function of isolated aortic rings of rats. Cadmium did not modify the acetylcholine-induced relaxation. After L-NAME addition, the relaxation induced by acetylcholine was abolished in presence or absence of cadmium, suggesting that acutely, this metal did not change NO release. However, tetraethylammonium (a nonselective K+ channels blocker) reduced acetylcholine-induced relaxation but this effect was lower in the preparations with cadmium, suggesting a decrease of K+ channels function in acetylcholine response after cadmium incubation. Apamin (a selective blocker of small Ca2+-activated K+ channels—SKCa), iberiotoxin (a selective blocker of large-conductance Ca2+-activated K+ channels—BKCa), and verapamil (a blocker of calcium channel) reduced the endothelium-dependent relaxation only in the absence of cadmium. Finally, cadmium decreases Na+/K+-ATPase activity. Our results provide evidence that the cadmium acute incubation unaffected the calcium-activated potassium channels (SKCa and BKCa) and voltage-calcium channels on the acetylcholine vasodilatation. In addition, acute cadmium incubation seems to reduce the Na+/K+-ATPase activity. 相似文献
10.
Myogenic, or pressure-induced, vasoconstriction is critical for local blood flow autoregulation. Underlying this vascular smooth muscle (VSM) response are events including membrane depolarization, Ca2+ entry and mobilization, and activation of contractile proteins. Large conductance, Ca2+-activated K+ channel (BKCa) has been implicated in several of these steps including, (1) channel closure causing membrane depolarization, and (2) channel opening causing hyperpolarization to oppose excessive pressure-induced vasoconstriction. As multiple mechanisms regulate BKCa activity (subunit composition, membrane potential (Em) and Ca2+ levels, post-translational modification) tissue level diversity is predicted. Importantly, heterogeneity in BKCa channel activity may contribute to tissue-specific differences in regulation of myogenic vasoconstriction, allowing local hemodynamics to be matched to metabolic requirements. Knowledge of such variability will be important to exploiting the BKCa channel as a therapeutic target and understanding systemic effects of its pharmacological manipulation. 相似文献
11.
《Life sciences》1995,56(15):PL291-PL298
The aim of this study was to examine the effects of MCI-154, a new positive inotropic agent with vasodilating properties, on the Ca2+-activated K+ channel (KCa channel) of vascular smooth muscle cells. Cultured smooth muscle cells from a porcine coronary artery were studied using the patch-clamp technique. Extracellular application of 100 μM MCI-154 activated the KCa channel in intact cell-attached patch configurations. In excised inside-out patch configurations, application of 100μM MCI-154 to the cytosolic side activated the KCa channel directly, suggesting that the Ca2+ sensitivity of the KCa channel itself is modulated. Though extracellular application of 100 μM amrinone, a phosphodiesterase inhibitor, activated the KCa channel in the cell-attached patch configurations, application of 100 μm amrinone to the cytosolic side could not activate the KCa channel in inside-out patch configurations. These results indicate that different from amrinone, MCI-154 can modulate Ca2+ sensitivity of the KCa channel in vascular smooth muscle cells. 相似文献
12.
1. Ca2+-antagonists counteract the muscular activity of the sea urchin pluteus. Agents that block rapid Na+-channels have no effect.2. High muscular activity is induced by increasing the sea water concentration of Ca2+ or K+ and by a Ca2+-ionophore. The stimulatory effects tend to decline.3. Muscarinic agents counteract the effects of Ca2+ and K+.4. Variation in the concentration of Ca2+ or K+ has profound effects on the response to nicotinic agents.5. It is suggested that Ca2+ plays the role as a charge-carrier and in the release of monoamines from an inner source, and that an excessive Ca2+-influx induces an outflux of K+ leading to hyperpolarization and abolition of the impulse activity. 相似文献
13.
14.
《Channels (Austin, Tex.)》2013,7(3):174-180
Bupivacaine is a local anesthetic compound belonging to the amino amide group. Its anesthetic effect is commonly related to its inhibitory effect on voltage-gated sodium channels. However, several studies have shown that this drug can also inhibit voltage-operated K+ channels by a different blocking mechanism. This could explain the observed contractile effects of bupivacaine on blood vessels. Up to now, there were no previous reports in the literature about bupivacaine effects on large conductance voltage- and Ca2+-activated K+ channels (BKCa). Using the patch-clamp technique, it is shown that bupivacaine inhibits single-channel and whole-cell K+ currents carried by BKCa channels in smooth muscle cells isolated from human umbilical artery (HUA). At the single-channel level bupivacaine produced, in a concentration- and voltage-dependent manner (IC50 324 µM at +80 mV), a reduction of single-channel current amplitude and induced a flickery mode of the open channel state. Bupivacaine (300 µM) can also block whole-cell K+ currents (~45% blockage) in which, under our working conditions, BKCa is the main component. This study presents a new inhibitory effect of bupivacaine on an ion channel involved in different cell functions. Hence, the inhibitory effect of bupivacaine on BKCa channel activity could affect different physiological functions where these channels are involved. Since bupivacaine is commonly used during labor and delivery, its effects on umbilical arteries, where this channel is highly expressed, should be taken into account. 相似文献
15.
Ronghua ZhuGe Rongfeng Bao Kevin E. Fogarty Lawrence M. Lifshitz 《The Journal of biological chemistry》2010,285(3):2203-2210
Ca2+ sparks are short lived and localized Ca2+ transients resulting from the opening of ryanodine receptors in sarcoplasmic reticulum. These events relax certain types of smooth muscle by activating big conductance Ca2+-activated K+ channels to produce spontaneous transient outward currents (STOCs) and the resultant closure of voltage-dependent Ca2+ channels. But in many smooth muscles from a variety of organs, Ca2+ sparks can additionally activate Ca2+-activated Cl− channels to generate spontaneous transient inward current (STICs). To date, the physiological roles of Ca2+ sparks in this latter group of smooth muscle remain elusive. Here, we show that in airway smooth muscle, Ca2+ sparks under physiological conditions, activating STOCs and STICs, induce biphasic membrane potential transients (BiMPTs), leading to membrane potential oscillations. Paradoxically, BiMPTs stabilize the membrane potential by clamping it within a negative range and prevent the generation of action potentials. Moreover, blocking either Ca2+ sparks or hyperpolarization components of BiMPTs activates voltage-dependent Ca2+ channels, resulting in an increase in global [Ca2+]i and cell contraction. Therefore, Ca2+ sparks in smooth muscle presenting both STICs and STOCs act as a stabilizer of membrane potential, and altering the balance can profoundly alter the status of excitability and contractility. These results reveal a novel mechanism underlying the control of excitability and contractility in smooth muscle. 相似文献
16.
Yan Yang Peng-Yun LiJun Cheng Fang CaiMing Lei Xiao-Qiu TanMiao-Ling Li Zhi-Fei LiuXiao-Rong Zeng 《Biochemical and biophysical research communications》2013
Large conductance Ca2+-activated K+ channel (BKCa) is a potential target for coronary artery-relaxing medication, but its functional regulation is largely unknown. Here, we report that inositol trisphosphate (IP3) activated BKCa channels in isolated porcine coronary artery smooth muscle cells and by which decreased the coronary artery tone. Both endogenous and exogenous IP3 increased the spontaneous transient outward K+ currents (STOC, a component pattern of BKCa currents) in perforated and regular whole-cell recordings, which was dependent on the activity of IP3 receptors. IP3 also increased the macroscopic currents (MC, another component pattern of BKCa currents) via an IP3 receptor- and sarcoplasmic Ca2+ mobilization-independent pathway. In inside-out patch recordings, direct application of IP3 to the cytosolic side increased the open probability of single BKCa channel in an IP3 receptor-independent manner. We conclude that IP3 is an activator of BKCa channels in porcine coronary smooth muscle cells and exerts a coronary artery-relaxing effect. The activation of BKCa channels by IP3 involves the enhancement of STOCs via IP3 receptors and stimulation of MC by increasing the Ca2+ sensitivity of the channels. 相似文献
17.
Telezhkin V. S. Tsvilovskii V. V. Dyskina Yu. B. Davydovskaya N. V. Shuba M. F. 《Neurophysiology》2001,33(5):281-288
Using a sucrose-bridge technique, we studied electrical and mechanical responses of smooth muscle ring strips of the rabbit main pulmonary artery to applications of blockers of voltage-operated (including Ca2+-dependent) K+ channels, tetraethylammonium (TEA) and 4-aminopyridine (4-AP), as well to application of nitric oxide (NO); nitroglycerin (NG) was used as a donor of the latter. All experiments were carried out under conditions of blockade of the adreno- and cholinoreceptors in the preparation. Both TEA and 4-AP evoked dose-dependent effects: depolarization of smooth muscle cells (SMC) and their contraction. Simultaneous addition of TEA and 4-AP to the normal superfusate (Krebs solution) resulted in intensification of depolarization and initiated generation of action potentials (AP); contractions became rather intensive and possessed a tetanic pattern. Addition of NG to TEA- and 4-AP-containing Krebs solution effectively suppressed AP generation and contractions, whereas the depolarization level underwent only mild modifications. These findings show that Ca2+-dependent high-conductance K+ channels (KCa channels) and 4-AP-sensitive voltage-operated K+ channels (KV channels) are involved in the formation of the resting membrane potential (RMP) in SMC of the rabbit main pulmonary artery. The impact of the KCa channels is greater than that of the KV channels. We suppose that the effects of NO on SMC are related to inhibition of the activity of high-threshold voltage-operated L-type Ca2+ channels and, probably, to lowering of the sensitivity of the contractile SMC apparatus to Ca2+. 相似文献
18.
James W. Putney Jr. 《Cell calcium》1983,4(5-6)
In the rat parotid salivary gland, fluid secretion is regulated by alterations in fluxes of monovalent ions.
, stimulation of muscarinic, α-adrenergic or substance P receptors provokes a biphasic increase in membrane permeability to K+ which can be conveniently assayed as efflux of 86Rb. The increased 86Rb flux is thought to arise in response to a receptor mediated elevation in [Ca2+]i which activates Ca2+-activated K+-channels. The biphasic nature of the response is presumably due to a biphasic mode of Ca2+ mobilization by secretagogues; a transient response reflects release of a finite pool of Ca from an intracellular store while a more sustained phase results from Ca entry through receptor operated Ca channels or gates. Calcium also mediates an increased Na+ entry which in turn activates the Na+, K+-pump. The mechanism involved in the regulation of monovalent ion channels by Ca2+ is not understood. 相似文献
19.
Passive Glial Cells, Fact or Artifact? 总被引:3,自引:0,他引:3
Astrocytes that are recorded in acute tissue slices of rat hippocampus using whole-cell patch-clamp, commonly exhibit voltage-activated
Na+ and K+ currents. Some reports have described astrocytes that appear to lack voltage-activated currents and proposed that these cells
constitute a subpopulation of electrophysiologically passive astrocytes. We show here that these cells can spontaneously change
during a recording unmasking expression of previously suppressed voltage-activated currents, suggesting that such cells do
not represent a subpopulation of passive astrocytes. Superfusion of a low Ca2+/EGTA solution was able to reversibly suppress voltage-activated K+ currents in cultured astrocytes. Currents were restored upon addition of normal bath Ca2+. These effects of Ca2+ on both outward and inward K+ currents were dose- and time-dependent, with increasing concentrations of Ca2+ (from 0 to 800 μm) leading to a gradual unmasking of voltage-dependent outward and inward K+ currents. The transition from an apparently passive cell to one exhibiting prominent voltage-activated currents was not associated
with any changes in membrane capacitance or access resistance. By contrast, in cells in which low access resistance or poor
seal accounted for the absence of voltage-activated currents, improvement of cell access was always accompanied by changes
in series resistance and membrane capacitance.
We propose that spillage of pipette solution containing low Ca2+/EGTA during cell approach in slice recordings and/or poor cell access, lead to a transient masking of voltage-activated currents
even in astrocytes that express prominent voltage-activated currents. These cells, however, do not constitute a subpopulation
of electrophysiologically passive astrocytes.
Received: 22 April 1998/Revised: 8 September 1998 相似文献
20.
I. V. Shemarova K. V. Sobol’ S. M. Korotkov V. P. Nesterov 《Journal of Evolutionary Biochemistry and Physiology》2014,50(3):221-226
Inoptopic effect of yttrium acetate (Y3+) on myocardium of the marsh frog Rana ridibunda and its effect on ion transport across the inner mitochondrial membrane (IMM) of rat heart was studied. Y3+ was found to decrease the rate of heart contractions and to stimulate ion transport in the rat heart mitochondria in media with 10 mM glutamate and 2 mM malate. Presence of Y3+ induced inhibition of energy-dependent Ca2+ transport into mitochondria, which was expressed as a marked decrease of their swelling in the media containing 125 mM NH4NO3 and Ca2+ or 25 mM potassium acetate, 100 mM sucrose and Ca2+. It is suggested that the Y3+-induced decrease in rat muscle contractions is determined not only by direct suppressing effect of Y3+ on potential-modulated Ca2+-channels of pacemaker and contractile cardiomyocytes (CM), but also by its indirect effect on Ca2+-carrier in IMM. The data confirming that Y3+ activates energy-dependent K+ transport catalyzed by mitochondrial uniporter and blocks Ca2+-channels in the mitochondrial membrane are important for more complete understanding of mechanisms of the Y3+ action on vertebrates and human CM. 相似文献