Sodium current in ventricular myocardial fibers

Membrane currents were measured in thin bundles of dog ventricular myocardium under voltage-clamp conditions. A rather large initial inward current which had an equilibrium potential at about + 55 millivolts could be recorded. When the external sodium concentration was reduced, the equilibrium potential for this current was shifted by the amount predicted theoretically for a current carried solely by sodium ions. The size of the sodium inward current (I(Na)) was largely dependent on the preceding membrane potential. The I(Na) was completely inactivated if the membrane potential was as low as -45 millivolts. Sodium ions are the main carrier of charge during the rapid depolarization phase of the action potential.     

Strophanthidin-sensitive transport of cesium and sodium in muscle cells

Uptake of cesium-134 ions into muscle cells is reduced to very low values by the presence of 10(-5)M strophanthidin in the Ringer solution. Cesium ions can induce extrusion of sodium from muscle cells in which the intracellular sodium content is elevated. The cesium-induced extra efflux of sodium-22 is inhibited by the external presence of 10(-5)M strophanthidin. The coupling between inward movement of cesium and outward movement of sodium appears to be chemical in nature. The evidence suggests that cesium ions are transported into muscle cells by a system of sites or carriers that requires a source of metabolic energy for ion turnover to occur.     

Sodium-calcium exchange in heart: membrane currents and changes in [Ca2+]i

Recordings have been made of changes in intracellular calcium ion concentration ([Ca2+]i) that can be attributed to the operation of an electrogenic, voltage-dependent sodium-calcium (Na-Ca) exchanger in mammalian heart cells. Guinea pig ventricular myocytes under voltage clamp were perfused internally with fura-2, a fluorescent Ca2+-indicator, and changes in [Ca2+]i and membrane current that resulted from Na-Ca exchange were identified through the use of various organic channel blockers and impermeant ions. Depolarization of cells elicited slow increases in [Ca2+]i, with the maximum increase depending on internal [Na+], external [Ca2+], and membrane voltage. Repolarization was associated with net Ca2+ efflux and a decline in the inward current that developed instantaneously upon repolarization. The relation between [Ca2+]i and current was linear, and the slope was made steeper by hyperpolarization.     

The relationship between charge movements associated with ICa and INa-Ca in cardiac myocytes

Ventricular myocytes exhibit a nifedipine-sensitive inward calcium current (ICa) and contracture when they are voltage clamped from -40 to 0 millivolt in the presence of caffeine and in the absence of extracellular sodium. However, upon repolarization they fail to relax because neither the sarcoplasmic reticulum nor the sodium-calcium exchange can reduce intracellular calcium. Sudden application of extracellular sodium during the contracture (but after repolarization) causes immediate relaxation and activates a transient inward sodium-calcium exchange current (INa-Ca), whose peak slightly precedes mechanical relaxation. The total charge carried by the nifedipine-sensitive ICa is twice the total charge carried by the transient inward INa-Ca. Assuming an exchange stoichiometry of three sodium to one calcium, these results indicate that all the calcium entering the cell during the initial depolarization is extruded by the sodium-calcium exchange.     

Calcium and sodium channels in spontaneously contracting vascular muscle cells

Electrophysiological recordings of inward currents from whole cells showed that vascular muscle cells have one type of sodium channel and two types of calcium channels. One of the calcium channels, the transient calcium channel, was activated by small depolarizations but then rapidly inactivated. It was equally permeable to calcium and barium and was blocked by cadmium, but not by tetrodotoxin. The other type, the sustained calcium channel, was activated by larger depolarizations, but inactivated very little; it was more permeable to barium than calcium. The sustained calcium channel was more sensitive to block by cadmium than the transient channel, but also was not blocked by tetrodotoxin. The sodium channel inactivated 15 times more rapidly than the transient calcium channel and at more negative voltages. This sodium channel, which is unusual because it is only blocked by a very high (60 microM) tetrodotoxin concentration but not by cadmium, is the first to be characterized in vascular muscle, and together with the two calcium channels, provides a basis for different patterns of excitation in vascular muscles.     

Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells

In acinar cells from rat salivary glands, cholinergic agonists cause oscillations in cytoplasmic free calcium concentration, which then drive oscillations of cell volume that reflect oscillating cell solute content and fluid secretion. By quantitative fluorescence ratio microscopy of an intracellular indicator dye for sodium, it has now been shown that large amplitude oscillations of sodium concentration were associated with the calcium and cell volume oscillations. Both calcium and sodium oscillations were dependent on the continued presence of calcium in the extracellular medium and were abolished by the specific sodium-potassium adenosine triphosphatase inhibitor ouabain. Thus, calcium oscillations in salivary acinar cells, by modulating the activities of ion transport pathways in the plasma membrane, can cause significant oscillations of monovalent ions that may in turn feed back to regulate calcium oscillations and fluid secretion.     

Adrenaline: mechanism of action on the pacemaker potential in cardiac Purkinje fibers

The pacemaker potential in Purkinje fibers is generated by a slow fall in potassium current which allows the inward background currents to depolarize the membrane. Adrenaline shifts the relation between activation of the potassium current and membrane potential in a depolarizing direction. Consequently, during the pacemaker potential, the potassium current falls more rapidly to lower values and the inward currents then depolarize the membrane more quickly. The shift in the potassium activation curve produced by adrenaline is large compared to that produced by calcium ions. The molecular action of adrenaline may involve either a large change in the surface charge of the membrane or a change in the dependence of the potassium permeability on the local electric field.     

阴离子淀粉对土壤养分离子的吸附作用

减少养分的损失是控制面源污染最有效和经济的方法。通过淋溶试验评价带负电荷的阴离子淀粉对土壤养分离子的吸附作用,寻找对土壤养分离子吸附效果好的淀粉种类。试验1设置5个处理:去离子水、硝酸钾,以及硝酸钾分别与黄原酸酯淀粉、磷酸酯淀粉和羧甲基淀粉等3种不同淀粉混合;试验2设置去离子水、黄原酸酯淀粉、黄原酸酯淀粉和氯化铵混合、氯化铵等4个处理。阴离子淀粉取代度是决定它们对阳离子吸附强度的主要因子,供试的3种阴离子淀粉对土壤中的阳离子吸附作用高低顺序:羧甲基淀粉＞ 磷酸酯淀粉＞ 黄原酸酯淀粉。以黄原酸酯淀粉为载体,用氯化铵溶液处理结果表明:黄原酸酯淀粉对土壤中的钠、钾、镁和钙等4种阳离子均有显著的吸附作用(P＜0.05);而用硝酸钾溶液处理时,黄原酸酯淀粉对土壤中的钠离子、铵离子和钾离子吸附效果较好,而对钙、镁等2种离子的吸附效果不明显,说明淀粉对阳离子的吸附效果与加入的营养液也有很大的关系。阴离子淀粉对阴离子养分没有吸附作用。试验推测,具有较高取代度的黄原酸酯淀粉可作为理想的吸附剂,没有潜在风险;在降水量较小的地区,较高取代度的磷酸酯淀粉也可以作为理想的吸附剂,因为没有铵离子淋失的风险。     

Permeation of calcium ions through non-NMDA glutamate channels in retinal bipolar cells.

The conduction of calcium ions through glutamate-gated channels is important in the induction of long-term potentiation and may trigger other cellular changes. In retinal bipolar cells, which lack the N-methyl-D-aspartate (NMDA) type of glutamate-gated channel, calcium permeability through non-NMDA channels was examined. Changes in extracellular calcium concentration unexpectedly affected the reversal potential for glutamate-induced currents in a manner consistent with these channels being highly permeable to calcium. External magnesium ions promote desensitization of these non-NMDA channels in a voltage-independent way. Thus, in addition to non-NMDA channels that conduct only sodium and potassium, there is a class that is also permeable to calcium.     

Body temperature: possible ionic mechanism in the hypothalamus controlling the set point

The body temperature of many mammals is set at or around 37 degrees C. The mechanism for this set point appears to depend on a constant and inherent balance between sodium and calcium ions within the posterior hypothalamus. When this region is perfused in unanesthetized cats, an extracellular excess or a normal physiological concentration of sodium ions evokes a rise in body temperature if calcium is not in the perfusate. At the same site, an excess or normal concentration of calcium ions causes the temperature to fall when sodium is absent.     

超高压下Ca~(2+)与Na~+离子对甜菜果胶结构及流变性质的影响

[目的]研究超高压下不同浓度Ca2+与Na+对甜菜果胶结构及流变性质的影响,为甜菜果胶在食品中的应用提供理论依据。[方法]甜菜果胶用浓度0.05 mol·L-1的Tris-HCl溶液溶解,添加不同浓度Ca2+(2、12和20mmol·L-1)和Na+(0.05、0.1和0.6 mol·L-1),配制成1%(w/v)甜菜果胶溶液后进行超高压处理,然后分别对甜菜果胶分子量、微观结构、黏度和动态粘弹性进行测定。[结果]与常压下相比,在450 MPa条件下处理不同时间(10、20、30和50 min)后,甜菜果胶在1 550 cm-1处均出现新的吸收峰,甜菜果胶溶液的屈服应力σ0显著增加,但不同超高压处理时间之间无显著差异。添加不同浓度Ca2+或Na+的甜菜果胶在450 MPa条件下处理30 min,其结构及流变性的变化有所不同。相对于未添加Ca2+或Na+的甜菜果胶,添加2 mmol·L-1 Ca2+离子使甜菜果胶溶液屈服应力σ0、储能模量G’和损耗模量G"均明显增加,当Ca2+浓度增加到12 mmol·L-1和20 mmol·L-1时,果胶的流变性质变化不显著;添加2 mmol·L-1 Ca2+使甜菜果胶分子发生明显的交联。果胶分子量由只高压处理的2.25×105 Da显著增加到6.07×105 Da,Ca2+的添加浓度增加到20 mmol·L-1,果胶的分子量变为5.99×105 Da,与添加2mmol·L-1 Ca2+时没有显著差异,其流变性质变化亦不显著。相对于未添加Ca2+或Na+的甜菜果胶,添加0.05 mol·L-1 Na+也使甜菜果胶的屈服应力σ0显著增加,并且随着Na+浓度的持续增加,果胶的屈服应力σ0显著增加;而只有当Na+浓度增加到0.6 mol·L-1时,甜菜果胶储能模量G’和损耗模量G"才发生明显增加。添加0.1 mmol·L-1 Na+的甜菜果胶,其果胶分子链相互交联成网状,果胶分子发生明显聚集,果胶分子量显著增加到11.95×105 Da;而当Na+浓度增加到0.6 mol·L-1时,果胶链呈棒状结构,果胶分子量显著降低到5.53×105 Da。[结论]超高压下Ca2+与Na+可能与甜菜果胶分子结合使其结构发生改变,进而影响甜菜果胶的结构及流变性质。     

海藻酸钠包埋的酵母菌转化人参皂苷Rb1的研究

为探索海藻酸钠包埋酵母菌转化人参皂苷Rb1的最佳条件,选用浓度为1.25×108个·mL-1的酵母菌菌悬液进行包埋,使用紫外分光光度计测定发酵液中人参皂苷Rb1含量变化计算生物转化率。通过单因素和正交设计试验分别考察海藻酸钠浓度、包埋时间、接种量和CaCl2浓度对所包埋的酵母菌转化人参皂苷的影响,最终获得了海藻酸钠包埋酵母菌转化人参皂苷Rb1的最佳条件为包埋时间45min,接种量7%,海藻酸钠浓度5%,CaCl2浓度10%。在该条件下,所包埋酵母菌对人参皂苷Rb1的最高生物转化率为31.51%,较以往未包埋的酵母菌转化人参皂苷Rb1的生物转化率提高约3%～5%。本研究首次利用海藻酸钠包埋酵母菌转化人参皂苷Rb1,解决了酵母菌种子不能重复使用等问题,简化了灭菌、菌种活化等步骤,为人参皂苷Rb1等苷类物质的高效生物转化提供了很好的思路和可借鉴的成功范例。     

Residual calcium ions depress activation of calcium-dependent current

Calcium ions enter and accumulate during depolarization of some cells, activating a potassium current, IK(Ca), that depends on the cytoplasmic concentration of calcium ions, [Ca]i. However, elevation of [Ca]i can depress IK(Ca) elicited by a subsequent membrane depolarization. The depression of IK(Ca) is ascribed here to a [Ca]i-mediated inactivation of the voltage-gated calcium conductance, which causes a net reduction in calcium ions available for the activation of IK(Ca). This suggests that other processes dependent on gated calcium entry may also be depressed by small background elevations in cytosolic free calcium ions.     

Sodium and potassium effects on skeletal muscle microsomal adenosine triphosphatase and calcium uptake

The relationship between the (Na(+) and K(+))-activated adenosine triphosphatase enzyme system implicated in sodium-transport by cell membranes and the calcium-activated adenosine triphosphatase, which is generally associated with calcium uptake, was examined in microsomes from skeletal muscle. Whereas sodium and potassium did not modify the relatively low adenosine triphosphatase activity seen in the absence of calcium, a pattern similar to that of the sodium-transport enzyme system was seen afer the addition of CaCl(2). The calcium-activated adenosine triphosphatase was stimulated equally by sodium or potassium alone, but both the rate and extent of calcium uptake were enhanced more by potassium than by sodium at concentrations below 0.12 mole per liter. In the absence of either of these ions addition of calcium failed to activate adenosine triphosphatase although significant amounts of calcium were taken up by the microsomes.     

Calcium requirement for melanophore-stimulating hormone action on melanophores

The calcium ion is specifically required for the action of melanophorestimulating hormone on melanosome dispersion within lizard (Anolis carolinensis) melanophores in vitro. The response to this hormone is directly related to the concentration of the Ca(2+) ion. Lithium, choline, rubidium, and cesium will replace the sodium and potassium of Ringer solution if Ca(2+) is present. Calcium ions are not required for melanosome dispersion itself, since theophylline or dibutyryl cyclic adenosine monophosphate reversibly darkens lizard skins in the absence of calcium.     

Calcium ion release in mechanically disrupted heart cells

In cardiac muscle fibers which have had their sarcolemma disrupted intracellular stores of calcium ions can be released by the same chemical stimuli which cause their release from the sarcoplasmic reticulum of skinned skeletal muscle fibers. These stimuli are increases in calcium or caffeine concentrations and substitution of chloride for propionate or sodium for potassium in solutions bathing the fibers.     

Ionic mobility in muscle cells

The diffusivities of ionic potassium, sodium, sulfate, and adenosine triphosphate inside a nmuscle cell are reduced by a factor of 2, relative to diffusivities in aqueous solution. The diffusion coefficients of nonelectrolytes are reduced by the same factor, showing that the diffusion of the ions is retarded by physical, rather than chemical, interactions. In contrast, the diffusivity of the calcium ion, which is taken up by the sarcoplasmic reticulum, is reduced fiftyfold.     

Tetrodotoxin: effects on brain metabolism in vitro

A 3-micromolar concentration of tetrodotoxin completely inhibits the stimulation of respiration of rat brain cortex that takes place upon application of electrical impulses. It also inhibits increase in the rate of the respiration that occurs when calcium ions are omitted from the incubation medium. No effect of tetrodotoxin on brain respiration takes place when stimulation is brought about by the addition of 100 millimolar potassium chloride. Tetrodotoxin prevents the fall in the rate of oxidation of cerebral acetate that occurs during electrical stimulation but does not affect the increased rate of the oxidation that occurs in the presence of an increased concentration of potassium chloride. The data indicate that oxidation of cerebral acetate is diminished by influx of sodium ions, which is prevented by tetrodotoxin, and is increased by influx of potassium ions, which is unaffected by tetrodotoxin.     

Atrionatriuretic peptide transforms cardiac sodium channels into calcium-conducting channels

The atrionatriuretic peptide (ANP) is released from atrial cells in response to increased extracellular fluid volume and reduces sodium absorption by the kidney, thus reducing the blood volume. In this report, ANP suppressed the calcium and sodium currents in rat and guinea pig ventricular myocytes. The suppression of sodium current was caused by enhanced permeability of the sodium channel to calcium without significant changes in the kinetics or the tetrodotoxin sensitivity of the channel. Thus, ANP may regulate the sodium channel by altering its cationic selectivity site to calcium, thereby repressing the sodium current. The suppression of sodium and calcium channels and the resultant depressed excitability of the atrial cells may help to regulate ANP secretion.     

Reactivated triton-extracted models o paramecium: modification of ciliary movement by calcium ions

Triton-extracted models of Paramecium were reactivated to swim in solutions of adenosine triphosphate and magnesium ions. The cilia beat in the normal direction (toward the rear) when the calcium ion concentration was less than 10-(6)M, and they beat in the "reversed" direction (toward the front) when calcium ion concentration was raised above 10-(6)M. These results support the proposal that ciliary reversal, hence backward swimming, of live paramecia is mediated by an increased cytoplasmic calcium concentration around the ciliary system by calcium-dependent membrane responses to external stimuli.