Simulation analysis of intracellular Na+ and Cl- homeostasis during beta 1-adrenergic stimulation of cardiac myocyte

To quantitatively understand intracellular Na⁺ and Cl⁻ homeostasis as well as roles of Na⁺/K⁺ pump and cystic fibrosis transmembrane conductance regulator Cl⁻ channel (I_CFTR) during the β1-adrenergic stimulation in cardiac myocyte, we constructed a computer model of β1-adrenergic signaling and implemented it into an excitation-contraction coupling model of the guinea-pig ventricular cell, which can reproduce membrane excitation, intracellular ion changes (Na⁺, K⁺, Ca²⁺ and Cl⁻), contraction, cell volume, and oxidative phosphorylation. An application of isoproterenol to the model cell resulted in the shortening of action potential duration (APD) after a transient prolongation, the increases in both Ca²⁺ transient and cell shortening, and the decreases in both Cl⁻ concentration and cell volume. These results are consistent with experimental data. Increasing the density of I_CFTR shortened APD and augmented the peak amplitudes of the L-type Ca²⁺ current (I_CaL) and the Ca²⁺ transient during the β1-adrenergic stimulation. This indirect inotropic effect was elucidated by the increase in the driving force of I_CaL via a decrease in plateau potential. Our model reproduced the experimental data demonstrating the decrease in intracellular Na⁺ during the β-adrenergic stimulation at 0 or 0.5 Hz electrical stimulation. The decrease is attributable to the increase in Na⁺ affinity of Na⁺/K⁺ pump by protein kinase A. However it was predicted that Na⁺ increases at higher beating rate because of larger Na⁺ influx through forward Na⁺/Ca²⁺ exchange. It was demonstrated that dynamic changes in Na⁺ and Cl⁻ fluxes remarkably affect the inotropic action of isoproterenol in the ventricular myocytes.     

Actions of emigrated neutrophils on Na(+) and K(+) currents in rat ventricular myocytes

Interactions between neutrophils and the ventricular myocardium can contribute to tissue injury, contractile dysfunction and generation of arrhythmias in acute cardiac inflammation. Many of the molecular events responsible for neutrophil adhesion to ventricular myocytes are well defined; in contrast, the resulting electrophysiological effects and changes in excitation–contraction coupling have not been studied in detail. In the present experiments, rat ventricular myocytes were superfused with either circulating or emigrated neutrophils and whole-cell currents and action potential waveforms were recorded using the nystatin-perforated patch method. Almost immediately after adhering to ventricular myocytes, emigrated neutrophils caused a depolarization of the resting membrane potential and a marked prolongation of myocyte action potential. Voltage clamp experiments demonstrated that following neutrophil adhesion, there was (i) a slowing of the inactivation of a TTX-sensitive Na⁺ current, and (ii) a decrease in an inwardly rectifying K⁺ current.

One cytotoxic effect of neutrophils appears to be initiated by enhanced Na⁺ entry into the myocytes. Thus, manoeuvres that precluded activation of Na⁺ channels, for example holding the membrane potential at −80 mV, significantly increased the time to cell death or prevented contracture entirely. A mathematical model for the action potential of rat ventricular myocytes has been modified and then utilized to integrate these findings. These simulations demonstrate the marked effects of (50-fold) slowing of the inactivation of 2–4% of the available Na⁺ channels on action potential duration and the corresponding intracellular Ca²⁺ transient. In ongoing studies using this combination of approaches, are providing significant new insights into some of the fundamental processes that modulate myocyte damage in acute inflammation.     

Ca entry through the store-mediated pathway directly activates only the K current but the subsequent Ca release from the store activates both K and Cl currents in submandibular gland acinar cells of the rat

The store-mediated Ca²⁺ entry was detected in single and cluster of rat submandibular acinar cells by measuring the Ca²⁺ activated ionic membrane currents. In the cells where intracellular Ca²⁺ was partly depleted by stimulation with submaximal concentration of acetylcholine (ACh) under a Ca²⁺-free extracellular condition, an employment of external Ca²⁺ in the absence of ACh caused a sustained increase of the K⁺ current without affecting the Cl⁻ current. A renewed ACh challenge without external Ca²⁺ caused repetitive spikes of both K⁺ and Cl⁻ currents due to the Ca²⁺ release. SK & F 96365 inhibited the generation of the sustained K⁺ current and refilling of the Ca²⁺ store following the Ca²⁺ readmission. It is suggested that the Ca²⁺ enters the cell through the store-mediated pathway near the K⁺ channels and is taken up by the store. Thus, only Ca²⁺ released from the store can activate both the K⁺ and Cl⁻ currents.     

A model of the guinea-pig ventricular cardiac myocyte incorporating a transverse-axial tubular system

A model of the guinea-pig cardiac ventricular myocyte has been developed that includes a representation of the transverse–axial tubular system (TATS), including heterogeneous distribution of ion flux pathways between the surface and tubular membranes. The model reproduces frequency-dependent changes of action potential shape and intracellular ion concentrations and can replicate experimental data showing ion diffusion between the tubular lumen and external solution in guinea-pig myocytes. The model is stable at rest and during activity and returns to rested state after perturbation. Theoretical analysis and model simulations show that, due to tight electrical coupling, tubular and surface membranes behave as a homogeneous whole during voltage and current clamp (maximum difference 0.9 mV at peak tubular I_Na of −38 nA). However, during action potentials, restricted diffusion and ionic currents in TATS cause depletion of tubular Ca²⁺ and accumulation of tubular K⁺ (up to −19.8% and +3.4%, respectively, of bulk extracellular values, at 6 Hz). These changes, in turn, decrease ion fluxes across the TATS membrane and decrease sarcoplasmic reticulum (SR) Ca²⁺ load. Thus, the TATS plays a potentially important role in modulating the function of guinea-pig ventricular myocyte in physiological conditions.     

Do stretch-induced changes in intracellular calcium modify the electrical activity of cardiac muscle?

Stretch of the myocardium influences the shape and amplitude of the intracellular Ca²⁺([Ca²⁺]_i) transient. Under isometric conditions stretch immediately increases myofilament Ca²⁺ sensitivity, increasing force production and abbreviating the time course of the [Ca²⁺]_i transient (the rapid response). Conversely, muscle shortening can prolong the Ca²⁺ transient by decreasing myofilament Ca²⁺ sensitivity. During the cardiac cycle, increased ventricular dilation may increase myofilament Ca²⁺ sensitivity during diastolic filling and the isovolumic phase of systole, but enhance the decrease in myofilament Ca²⁺ sensitivity during the systolic shortening of the ejection phase. If stretch is maintained there is a gradual increase in the amplitude of the Ca²⁺ transient and force production, which takes several minutes to develop fully (the slow response). The rapid and slow responses have been reported in whole hearts and single myocytes. Here we review stretch-induced changes in [Ca²⁺]_i and the underlying mechanisms.

Myocardial stretch also modifies electrical activity and the opening of stretch-activated channels (SACs) is often used to explain this effect. However, the myocardium has many ionic currents that are regulated by [Ca²⁺]_i and in this review we discuss how stretch-induced changes in [Ca²⁺]_i can influence electrical activity via the modulation of these Ca²⁺-dependent currents. Our recent work in single ventricular myocytes has shown that axial stretch prolongs the action potential. This effect is sensitive to either SAC blockade by streptomycin or the buffering of [Ca²⁺]_i with BAPTA, suggesting that both SACs and [Ca²⁺]_i are important for the full effects of axial stretch on electrical activity to develop.     

Physiological modulation of voltage-dependent inactivation in the cardiac muscle L-type calcium channel: a modelling study

The inactivation of the L-type Ca²⁺ current is composed of voltage-dependent and calcium-dependent mechanisms. The relative contribution of these processes is still under dispute and the idea that the voltage-dependent inactivation could be subject to further modulation by other physiological processes had been ignored. This study sought to model physiological modulation of inactivation of the current in cardiac ventricular myocytes, based upon the recent detailed experimental data that separated total and voltage-dependent inactivation (VDI) by replacing extracellular Ca²⁺ with Mg²⁺ and monitoring L-type Ca²⁺ channel behaviour by outward K⁺ current flowing through the channel in the absence of inward current flow. Calcium-dependent inactivation (CDI) was based upon Ca²⁺ influx and formulated from data that was recorded during β-adrenergic stimulation of the myocytes. Ca²⁺ influx and its competition with non-selective monovalent cation permeation were also incorporated into channel permeation in the model. The constructed model could closely reproduce the experimental Ba²⁺ and Ca²⁺ current results under basal condition where no β-stimulation was added after a slight reduction of the development of fast voltage-dependent inactivation with depolarization. The model also predicted that under β-adrenergic stimulation voltage-dependent inactivation is lost and calcium-dependent inactivation largely compensates it. The developed model thus will be useful to estimate the respective roles of VDI and CDI of L-type Ca²⁺ channels in various physiological and pathological conditions of the heart which would otherwise be difficult to show experimentally.     

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL-1 cells that is correlated with CRAC channel activation

Highly Ca²⁺ selective Ca²⁺ channels activated by store depletion have been recently described in several cell types and have been termed CRAC channels (for calcium release-activated calcium). The present study shows that following store depletion in mast and RBL-1 cells, monovalent outward currents could be recorded if the internal solution contained K⁺ but not Cs⁺. The activation of the outward K⁺ current correlated with the activation of I_CRAC, in both time and amplitude, suggesting that the K⁺ current might be carried by CRAC channels. The amplitude of the outward current was increased if external Ca²⁺ was reduced or replaced by external Ba²⁺. The outward K⁺ conductance might have a physiological role in maintaining the driving force for Ca²⁺ entry during the activation of CRAC channels.     

Fluoxetine-induced inhibition of synaptosomal [H] 5-HT release: Possible CA-channel inhibition

Fluoxetine, a selective 5-HT uptake inhibitor, inhibited 15 mM K⁺-induced [³H] 5-HT release from rat spinal cord and cortical synaptosomes at concentrations > 0.5 uM. This effect reflected a property shared by another selective 5-HT uptake inhibitor paroxetine but not by less selective uptake inhibitors such as amitriptyline, desipramine, imipramine or nortriptyline. Inhibition of release by fluoxetine was inversely related to both the concentration of K⁺ used to depolarize the synaptosomes and the concentration of external Ca²⁺. Experiments aimed at determining a mechanism of action revealed that fluoxetine did not inhibit voltage-independent release of [³H] 5-HT release induced by the Ca²⁺-ionophore A 23187 or Ca²⁺-independent release induced by fenfluramine. Moreover the 5-HT autoreceptor antagonist methiothepin did not reverse the inhibitory actions of fluoxetine on K⁺-induced release. Further studies examined the effects of fluoxetine on voltage-dependent Ca²⁺ channels and Ca²⁺ entry. Whereas fluoxetine and paroxetine inhibited binding of [³H] nitrendipine to the dihydropyridine-sensitive L-type Ca²⁺ channel, the less selective uptake inhibitors did not alter binding. The dihydropyridine antagonist nimodipine partially blocked fluoxetine-induced inhibition of release. Moreover enhanced K⁺-stimulated release due to the dihydropyridine agonist Bay K 8644 was reversed by fluoxetine. Fluoxetine also inhibited the K⁺-induced increase in intracellular free Ca²⁺ in fura-2 loaded synaptosomes. These data are consistent with the suggestion that fluoxetine inhibits K⁺-induced [³H] 5-HT release by antagonizing voltage-dependent Ca²⁺ entry into nerve terminals.     

'Ca(2+)-induced Ca(2+) entry' or how the L-type Ca(2+) channel remodels its own signalling pathway in cardiac cells

The adjustment of Ca²⁺ entry in cardiac cells is critical to the generation of the force necessary for the myocardium to meet the physiological needs of the body. In this review, we present the concept that Ca²⁺ can promote its own entry through Ca²⁺ channels by different mechanisms. We refer to it under the general term of ‘Ca²⁺-induced Ca²⁺ entry’ (CICE). We review short-term mechanisms (usually termed facilitation) that involve a stimulating effect of Ca²⁺ on the L-type Ca²⁺ current (I_Ca-L) amplitude (positive staircase) or a lessening of Ca²⁺-dependent inactivation of I_Ca-L. This latter effect is related to the amount of Ca²⁺ released by ryanodine receptors (RyR2) of the sarcoplasmic reticulum (SR). Both effects are involved in the control of action potential (AP) duration. We also describe a long-term mechanism based on Ca²⁺-dependent down-regulation of the Kv4.2 gene controlling functional expression of the repolarizing transient outward K⁺ current (I_to) and, thereby, AP duration. This mechanism, which might occur very early during the onset of hypertrophy, enhances Ca²⁺ entry by maintaining Ca²⁺ channel activation during prolonged AP. Both Ca²⁺-dependent facilitation and Ca²⁺-dependent down-regulation of I_to expression favour AP prolongation and, thereby, promote sustained voltage-gated Ca²⁺ entry used to enhance excitation–contraction (EC) coupling (with no change in the density of Ca²⁺ channels per se). These self-maintaining mechanisms of Ca²⁺ entry have significant functions in remodelling Ca²⁺ signalling during the cardiac AP. They might support a prominent role of Ca²⁺ channels in the establishment and progression of abnormal Ca²⁺ signalling during cardiac hypertrophy and congestive heart failure.     

Insulin secretion and intracellular Ca rises in monolayer cultures of neonatal rat β-cells

Glucose-induced insuline release, glucose-induced rises in intracellular free Ca²⁺ concentration ([Ca²⁺]_i), and voltage-dependent Ca²⁺ channel activity were assessed in monolayer cultures of β-vells 3–5 day-old rats. The glucose-stimulated insulin secretory responses and [Ca²⁺]_i rises were like those in adult rat β-cells rather than fetal rat β-cells. Voltage-dependent Ca²⁺ channel antagonists decreased glucose-induced insulin secretion, aborted the [Ca²⁺]₂ rise and, like deprivation of extracellular Ca²⁺, prevented the glucose-induced rise in [Ca²⁺]_i when added before the glucose challenge. The presence of nifedipine-sensitive, voltage-dependent Ca²⁺ channels was demonstrated directly by measuring Ca²⁺ currents using the whole-cell configuration of the patch-clamp technique and indirectly by measuring [Ca²⁺]₁ after membrane depolarization by 45 mMm K⁺ or 200 μM tolbutamide. Thus, in cultured β-cells of 3–5 day-old rats the coupling of glucose stimulation to Ca²⁺ influx is essentially mature, in contrast to what has been reported for fetal or very early neonatal cells.     

Inhibition of cell growth by K channel modulators is due to interference with agonist-induced Ca release

The effects of K⁺ channel modulators, tetraethylammonium, 4-aminopyridine and diazoxide, and high extracellular K⁺ on cell growth and agonist-induced intracellular Ca²⁺ mobilization were investigated. Two human brain tumour cell lines, U-373 MG astrocytoma and SK-N-MC neuroblastoma, were used as model cellular systems. K⁺ channel modulators and increased extracellular K⁺ concentration inhibited tumour cell growth in a dose-related fashion in both cell lines. In addition, agonist (carbachol or serum)-induced intracellular Ca²⁺ mobilization was also blocked by the pretreatment of growth-inhibitory concentrations of K⁺ channel modulators and high extracellular K⁺. Thus, these results suggest that K⁺ channel modulators are effective inhibitors of brain tumour cell growth and that their growth regulation may be due to the interference with the intracellular Ca²⁺ signalling mechanisms.     

Characterization of Acetylcholine-induced Increases in Cytosolic Free Calcium Concentration in Individual Rat Pancreatic β-cells

The intracellular free Ca²⁺ ion concentration ([Ca²⁺]i) was measured using fura-2 microspec-trofluorimetry in individual rat pancreatic β-cells prepared by enzymatic digestion and fluorescence-activated cell sorting. The mean basal concentration of [Ca²⁺]i in β-cells in the presence of 4.4 mM glucose and 1.8 mM Ca²⁺ was 112±1.6 nM (n=207). The action of acetylcholine (ACh) was concentration-dependent, and raising the concentration resulted in [Ca²⁺]i spikes of increasing amplitude and duration in some, but not all of the β-cells. In addition, the β-cells demonstrated variable sensitivity to ACh. The increases in [Ca²⁺]i were rapid, transient and were blocked by atropine at 10^-6M. A brief exposure to 50 mM K⁺ resulted in a transient increase in [Ca²⁺]i similar to that induced by ACh, but resistant to atropine. A high concentration of ACh (100μL 10^-4M or 10^-3M) induced [Ca²⁺]i oscillations in 11 out of 57 β-cells in the presence of 4.4 mM glucose. Using calcium channel blockers and Ca²⁺ free medium, the source of the increase in [Ca²⁺]i was deduced to be from extracellular spaces. Changing the temperature from 22 to 37°C did not affect the action of ACh on [Ca²⁺]i. These data strongly suggest that ACh exerted a direct action on [Ca²⁺]i in normal rat pancreatic β-cells and support a role for Ca²⁺ as a second messenger in the action of ACh.     

The blocking effect of BmP02, one novel short-chain scorpion peptide on transient outward K(+) channel of adult rat ventricular myocyte

Two components F-2-7-4 and F-2-7-5, each composed of 28 amino acid residues, were purified from the venom of Buthus martensi Karsch by an opportune procedure with cation-exchange column chromatography and repeated HPLC. Both components were totally accounted to about 0.88% dry weight of the crude venom.The molecular weights of both components were determined to be 2950 and 2935 by mass spectrometry, which were fully coincidence with that of the known novel short-chain peptides BmP02 and BmP03, respectively [Romi-Lebrun R, Martin-Eauclaire M-F, Escoubas P, Wu FQ, Lebrun B, Hisada M, Nakajima T. Characterization of four toxins from Buthus martensi scorpion venom, which act on apamin-sensitive Ca²⁺-activated K⁺ channels. Eur J Biochem 1997;145:457–464]. In addition, the sequence of component F-2-7-4 was analyzed to be the same as that of BmP02. The components F-2-7-4 and F-2-7-5 purified in this study were, thus, finally distinguished to be BmP02 and BmP03 from the same venom. Using whole cell patch-clamp recording, it was found that BmP02 diminished the current of transient outward K⁺ channel in adult rat ventricular myocyte in a concentration-dependent manner. The inhibitory effect was reversible. Dynamic studies showed that the activation, inactivation and recovery processes of the transient outward K⁺ channel were not changed significantly after applying of BmP02. In addition, when BmP02 was applied to guinea pig ventricular myocyte, both delayed and inward rectified K⁺ currents showed no change compared with the control. The results suggest strongly that BmP02 or -like peptides from scorpion venom may provide a useful probe for the studying of transient outward K⁺ channel in rat ventricular myocyte.     

细胞外Ba2+对大鼠心肌细胞L型钙通道的影响

目的：观察细胞外Ba²⁺对记录大鼠心肌细胞L型钙通道的影响。方法：采用急性酶解分离法获得大鼠的单个心肌细胞,使用全细胞膜片钳技术记录L型钙通道电流。采用Ba²⁺替换台式液中的Ca²⁺和直接向台式液中加入Ba²⁺（0~8 mmol/L）,观察峰值电流15 min内的变化,数据采用5个以上细胞进行重复。结果：（1）台式液中的Ca²⁺被Ba²⁺替换后,L型钙通道电流的失活速率明显减慢（P<0.01）;在台式液中加入少量Ba²⁺（0.2,0.4 mmol/L）时L型钙通道电流的失活速率无明显改变（P>0.05）,加入0.8 mmol/L Ba²⁺时失活速率明显减慢（P<0.05）。（2）与正常台式液比较,在细胞外液中加入Ba²⁺（0.2,0.4 mmol/L）峰值电流衰减减弱,其中10 min和15 min两个时间点衰减差异明显（P<0.01）。（3）在细胞外液中加入Ba²⁺可下移电流电压曲线,改变翻转电位,减弱丹酚酸A对钙电流的抑制强度,使量效关系曲线右移。结论：在细胞外液中加入一定浓度的Ba²⁺,能够减弱全细胞膜片钳技术记录大鼠心室肌细胞L型钙通道时出现的峰值电流衰减,改变通道的电压依赖特性,影响药物量效关系。     

严重烫伤延长大鼠心室肌细胞动作电位时程的机制

严重烫伤引起心肌细胞动作电位时程（action potential duration,APD）延长,通过加重烫伤心肌细胞钙紊乱和诱发室性心律失常,促进烫伤心功能障碍的发生,但APD延长的机制尚不清楚。通过制作约40％体表面积（total body surface area,TBSA）Ⅲ度烫伤大鼠模型,在伤后12h大鼠心功能明显减弱时分离其心肌细胞,采用膜片钳技术观察心肌细胞APD以及动作电位复极化相关的重要离子通道电流,包括瞬间外向钾电流（transient outward K^＋ current,Ito）,L-型钙电流（L-type Ca^2＋ current,ICa-L）和内向整流钾电流（inward rectifier K^＋ current,IK1）。结果显示,烫伤后12h单个心肌细胞APD明显延长,APD50和APD90在烫伤组分别为（46．02±3．78）ms、（123．24±12．48）ms（n=19）,明显长于对照组的（23．28±4．85）ms、（72．12±3．57）ms（n=17）（P〈0．01）。烫伤引起,Ito电流密度降低,＋60 mV下烫伤组的电流密度（20．39±1．98）pA／pF（n=25）明显低于对照组的（34．15±3．78）pA／pF（n=20,P〈0．01）;烫伤组在-120至-80mV电压刺激下所产生的IK1电流密度显著低于对照组：而两组之间ICa-L电流密度、电压依赖性的激活和失活无显著性差异。结果提示,烫伤引起心肌细胞APD延长的机制与瞬间外向钾通道和内向整流钾通道功能下调有关。     

盐胁迫下外源褪黑素和Ca2+对甜瓜幼苗的缓解效应

以甜瓜品种‘羊角酥瓜’为试材,利用人工气候室控制环境条件(昼/夜25/18 ℃),研究盐胁迫条件下外源褪黑素(MT)和Ca²⁺对甜瓜幼苗根系和叶片中Cl^-、Na⁺、K⁺、Mg²⁺、Ca²⁺离子含量,Na⁺/K⁺、 Na⁺/Ca²⁺、Na⁺/Mg²⁺值,以及H⁺-ATP酶活性、渗透调节物质积累和细胞膜质过氧化的影响.结果表明: 与对照相比,盐胁迫处理显著抑制甜瓜幼苗生长,增加根系和叶片中Cl^-、Na⁺含量,降低K⁺、Mg²⁺、Ca²⁺含量.盐胁迫下,喷施外源MT或Ca²⁺处理均可以显著降低甜瓜根系和叶片中Cl^-、Na⁺含量,提高K⁺、Mg²⁺、Ca²⁺含量,植株体内Na⁺/K⁺、Na⁺/Ca²⁺和 Na⁺/Mg²⁺值下降;同时也提高了根系和叶片H⁺-ATP酶活性及叶片渗透调节物质的含量,降低盐胁迫对细胞膜的伤害,表现在甜瓜叶片相对电导率和丙二醛含量降低.总之,在盐胁迫条件下,外源MT、Ca²⁺单独和复配处理均可通过提高H⁺-ATP酶活性来降低盐害离子的含量,改善甜瓜幼苗中的离子平衡,同时增加渗透调节物质的含量,降低膜质过氧化水平,从而增强其对盐胁迫的适应性,其中MT和Ca²⁺复配处理时的效果更好.复配外施 MT 和Ca²⁺在诱导甜瓜幼苗提高耐盐方面具有协同增效作用.     

The BK channel: a vital link between cellular calcium and electrical signaling

Large-conductance Ca²⁺-activated K⁺ channels (BK channels) constitute an key physiological link between cellular Ca²⁺ signaling and electrical signaling at the plasma membrane. Thus these channels are critical to the control of action potential firing and neurotransmitter release in several types of neurons, as well as the dynamic control of smooth muscle tone in resistance arteries, airway, and bladder. Recent advances in our understanding of K⁺ channel structure and function have led to new insight toward the molecular mechanisms of opening and closing (gating) of these channels. Here we will focus on mechanisms of BK channel gating by Ca²⁺, transmembrane voltage, and auxiliary subunit proteins.     

钙对盐胁迫下冰叶日中花不同器官离子含量和根部K~+、Na~+吸收的影响

以冰叶日中花(Mesembryanthemum crystallinum L.)实生苗为材料,经NaCl、NaCl+ CaCl_2、NaCl+LaCl_3处理后,利用电感耦合等离子发射光谱仪检测叶、茎、根中Na~+、K~+、Ca~(2+)、Mg~(2+)含量,计算K~+/Na~+、Ca~(2+)/Na~+和Mg~(2+)/Na~+比值,利用非损伤微测技术测定根尖Na~+流和K~+流,研究盐胁迫下钙在维持离子平衡中的作用。结果显示,NaCl处理后,冰叶日中花各器官中Na~+含量增加,K~+、Ca~(2+)、Mg~(2+)含量降低,离子比值降低;CaCl_2处理降低了Na~+含量,提高了K~+、Ca~(2+)、Mg~(2+)含量,离子比值升高,而LaCl_3处理后的结果相反。经NaCl处理24 h后,冰叶日中花根尖Na~+和K~+明显外流,加入CaCl_2后,Na~+外流速度显著增加,K~+外流速度受到抑制,而加入LaCl_3后则降低了Na~+的外流速度,促进了K~+的外流。研究结果表明冰叶日中花受到盐胁迫后,钙参与了促进根部Na~+外排、抑制K~+外流的过程,进而保持各器官中较低的Na~+含量,表明钙在维持和调控离子平衡中起到重要作用。     

盐胁迫下外源褪黑素和Ca2+对甜瓜幼苗的缓解效应

以甜瓜品种‘羊角酥瓜’为试材,利用人工气候室控制环境条件(昼/夜25/18 ℃),研究盐胁迫条件下外源褪黑素(MT)和Ca²⁺对甜瓜幼苗根系和叶片中Cl^-、Na⁺、K⁺、Mg²⁺、Ca²⁺离子含量,Na⁺/K⁺、 Na⁺/Ca²⁺、Na⁺/Mg²⁺值,以及H⁺-ATP酶活性、渗透调节物质积累和细胞膜质过氧化的影响.结果表明: 与对照相比,盐胁迫处理显著抑制甜瓜幼苗生长,增加根系和叶片中Cl^-、Na⁺含量,降低K⁺、Mg²⁺、Ca²⁺含量.盐胁迫下,喷施外源MT或Ca²⁺处理均可以显著降低甜瓜根系和叶片中Cl^-、Na⁺含量,提高K⁺、Mg²⁺、Ca²⁺含量,植株体内Na⁺/K⁺、Na⁺/Ca²⁺和 Na⁺/Mg²⁺值下降;同时也提高了根系和叶片H⁺-ATP酶活性及叶片渗透调节物质的含量,降低盐胁迫对细胞膜的伤害,表现在甜瓜叶片相对电导率和丙二醛含量降低.总之,在盐胁迫条件下,外源MT、Ca²⁺单独和复配处理均可通过提高H⁺-ATP酶活性来降低盐害离子的含量,改善甜瓜幼苗中的离子平衡,同时增加渗透调节物质的含量,降低膜质过氧化水平,从而增强其对盐胁迫的适应性,其中MT和Ca²⁺复配处理时的效果更好.复配外施 MT 和Ca²⁺在诱导甜瓜幼苗提高耐盐方面具有协同增效作用.     

Role of stretch-activated channels on the stretch-induced changes of rat atrial myocytes

The role of stretch-activated channels (SACs) on the stretch-induced changes of rat atrial myocytes was studied using a computer model that incorporated various ion channels and transporters including SACs. A relationship between the extent of the stretch and the activation of SACs was formulated in the model based on experimental findings to reproduce changes in electrical activity and Ca²⁺ transients by stretch. Action potentials (APs) were significantly changed by the activation of SACs in the model simulation. The duration of the APs decreased at the initial fast phase and increased at the late slow phase of repolarisation. The resting membrane potential was depolarised from −82 to −70 mV. The Ca²⁺ transients were also affected. A prolonged activation of SACs in the model gradually increased the amplitude of the Ca²⁺ transients. The removal of Ca²⁺ permeability through SACs, however, had little effect on the stretch-induced changes in electrical activity and Ca²⁺ transients in the control condition. In contrast, the removal of the Na⁺ permeability nearly abolished these stretch-induced changes. Plotting the peaks of the Ca²⁺ transients during the activation of the SACs along a time axis revealed that they follow the time course of the Na_i⁺ concentration. The Ca²⁺ transients were not changed when the Na_i⁺ concentration was fixed to a control value (5.4 mM). These results predicted by the model suggest that the influx of Na⁺ rather than Ca²⁺ through SACs is more crucial to the generation of stretch-induced changes in the electrical activity and associated Ca²⁺ transients of rat atrial myocytes.