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.     

Imaging elemental distribution and ion transport in cultured cells with ion microscopy

Both elemental distribution and ion transport in cultured cells have been imaged by ion microscopy. Morphological and chemical information was obtained with a spatial resolution of approximately 0.5 micron for sodium, potassium, calcium, and magnesium in freeze-fixed, cryofractured, and freeze-dried normal rat kidney cells and Chinese hamster ovary cells. Ion transport was successfully demonstrated by imaging Na+-K+ fluxes after the inhibition of Na+- and K+ -dependent adenosine triphosphatase with ouabain. This method allows measurements of elemental (isotopic) distribution to be related to cell morphology, thereby providing the means for studying ion distribution and ion transport under different physiological, pathological, and toxicological conditions in cell culture systems.     

Actomyosin-like protein isolated from mammalian brain

A protein with characteristics similar to actomyosin has been isolated from whole brain of rat and cat. It is soluble in 0.6 molar potassium chloride and insoluble in 0.1 molar potassium chloride. It superprecipitates with magnesium ions and adenosine triphosphate. It has adenosine triphosphatase activity stimulated by either magnesium or calcium ions. Both superprecipitation and adenosine triphosphatase activity are inhibited by p-chloromercuribenzoate and Mersalyl but not by ouabain.     

Cochlear function and sodium and potassium activated adenosine triphosphatase

The maintenance of the cation gradients between endolymph and perilymph in the cochlea requires the operation of a cation pump. An adenosine triphosphatase system activated by sodium and potassium is present in high activity in the cochlear membranes (tegmentum vasculosum and stria vascularis). The cochlear microphonic potential is inhibited by perilymphatic perfusion of ouabain and erythrophleine. Since the microphonic potential depends on the high concentration of potassium ions in the endolymph, our findings strongly suggest the operation of an adenosine triphosphatase cation pump system activated by sodium and potassium, in the generation of cochlear cation gradients.     

Erythrocyte abnormality in human myopathy

Erythrocyte ghosts isolated from myopathic patients responded to 10(-4) molar ouabain with a dramatic increase in adenosine triphosphatase activity, while identical preparations from normal donors were inhibited by the same drug. These results have been interpreted in terms of a disease-related change in membrane integrity bearing upon function of the transport enzyme.     

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.     

Regulation of erythrocyte cation and water content in sickle cell anemia

The pathophysiological events in sickle cell disease are critically dependent on the intracellular concentration of hemoglobin S, which varies inversely with cell cation and water content. Erythrocytes of SS homozygotes exposed to oxygen or carbon monoxide decrease their potassium and water content through a pathway for potassium transport that is activated by both cell swelling and decrease in internal pH. This pathway is not inhibited by ouabain either with or without bumetanide. When SS erythrocytes were separated according to density, the pH- and volume-dependent potassium transport was greatest in the least dense fraction and was reduced in the densest cells. This pathway, which does not depend on polymerization of sickle hemoglobin, may be important in regulating the cation and water content of SS erythrocytes.     

Methylation increases sodium transport into A6 apical membrane vesicles: possible mode of aldosterone action

When isolated apical membrane vesicles prepared from cultured A6 epithelia were incubated in vitro with the methyl donor S-adenosylmethionine, the control rate of amiloride-inhibitable sodium transport was doubled. The methylation inhibitors 3-deazaadenosine and S-adenosyl homocysteine returned the S-adenosyl-methionine-stimulated sodium transport to control levels. Neither these agents nor adenosine affected sodium transport into control vesicles. In vesicles incubated with S-adenosyl-[3H-methyl]methionine, both membrane phospholipids and proteins were labeled, and this labeling was inhibited by deazaadenosine. In vesicles prepared from A6 cells treated with aldosterone, sodium transport was twice the control value and S-adenosylmethionine did not cause any further stimulation of transport. In those vesicles, both lipid and protein methylation were increased. These results suggest that methylation, which increases the rate of amiloride-sensitive sodium transport is involved in the action of aldosterone at the apical membrane level in epithelia.     

Calmodulin activation of calcium-dependent sodium channels in excised membrane patches of Paramecium

Calmodulin is a calcium-binding protein that participates in the transduction of calcium signals. The electric phenotypes of calmodulin mutants of Paramecium have suggested that the protein may regulate some calcium-dependent ion channels. Calcium-dependent sodium single channels in excised patches of the plasma membrane from Paramecium were identified, and their activity was shown to decrease after brief exposure to submicromolar concentrations of calcium. Channel activity was restored to these inactivated patches by adding calmodulin that was isolated from Paramecium to the cytoplasmic surface. This restoration of channel activity did not require adenosine triphosphate and therefore, probably resulted from direct binding of calmodulin, either to the sodium channel itself or to a channel regulator that was associated with the patch membrane.     

Significance of tissue myo-inositol concentrations in metabolic regulation in nerve

Approximately 25 percent of resting energy utilization in isolated nerve endoneurium is inhibited by medium containing defatted albumin and selectively restored by arachidonic acid but is unaffected by indomethacin or nordihydroguaiaretic acid. The same component of energy utilization is inhibited by small decreases in endoneurial myo-inositol, which decrease incorporation of carbon-14-labeled arachidonic acid into phosphatidylinositol. The fraction of the resting oxygen uptake inhibited by ouabain is decreased 40 to 50 percent by a reduced tissue myo-inositol concentration or by defatted albumin. Metabolic regulation by rapid, basal phosphatidylinositol turnover is dependent on the maintenance of normal tissue myoinositol concentrations.     

Beta-adrenergic inhibition of cardiac sodium channels by dual G-protein pathways

The signaling pathways by which beta-adrenergic agonists modulate voltage-dependent cardiac sodium currents are unknown, although it is likely that adenosine 3'5'-monophosphate (cAMP) is involved. Single-channel and whole-cell sodium currents were measured in cardiac myocytes and the signal transducing G protein Gs was found to couple beta-adrenergic receptors to sodium channels by both cytoplasmic (indirect) and membrane-delimited (direct) pathways. Hence, Gs can act on at least three effectors in the heart: sodium channels, calcium channels, and adenylyl cyclase. The effect on sodium currents was inhibitory and was enhanced by membrane depolarization. During myocardial ischemia the sodium currents of depolarized cells may be further inhibited by the accompanying increase in catecholamine levels.     

DDT: inhibition of sodium chloride tolerance by the blue-green alga Anacystis nidulans

Anacystis nidulans, a freshwater blue-green alga, has been found to lerate sodium chloride (1 percent by weight) and DDT [1,1,1-trichloro-2,2-bis chlorophenyl) ethane] (800 parts per billion) separately, but growth was inhibited in the presence of both compounds. This inhibition was reversed by an increased calcium concentration. It is possible that inhibition of (Na+,K+)-activated adenosine triphosphatase) by DDT causes this species to lose the ability to lerate sodium chloride.     

Aspirin: its effect on platelet glycolysis and release of adenosine diphosphate

Incubation of human platelets with aspirin inhibited glycolysis and produced a fall in the concentration of adenosine triphosphate. When platelets were exposed to collagen there was an increase in glycolysis and release of adenosine diphosphate. Prior incubation of the platelets with aspirin for 5 minutes did not totally suppress the increase in glycolysis after exposure to collagen but completely inhibited the collagen-induced reaction of the release of adenosine diphosphate. It is suggested that aspirin acts on human platelets by inhibiting both release of adenosine diphosphate and the transport of glucose across the platelet membrane.     

Brush border particulates of renal tissue

Particulates containing a large part of the alkaline phosphatase activity of renal tissue were separated from homogenates and from ribosomal preparations by zonal centrifugation. The particles had a high content of phospholipid and cholesterol that was not removed by treatment with I percent deoxycholate. Enzymatic activities concentrated with the particles were the alkaline phosphatase, a peptidase resistant to proteolysis, glucose-6-phosphatase, inorganic pyrophos-phatase, and adenosine triphosphatase. The particles accumulated leucine with no stimulation from soluble factors and with inhibition by other amino acids; the accumulation was stimulated by adenosine triphosphate and was not inhibited by puromycin. The particles appear to be derived from the membranes of the brush borders of tubular cells.     

Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum

The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.     

Synaptic activation of an electrogenic sodium pump

An identified molluscan interneuron mediates different cholinergic synaptic actions by increasing the conductance of its follower cells to different ions. We have now found that this interneuron also mediates a new class of synaptic actions which does not involve a conductance change but the activation of an electrogenic sodium pump. This synaptic action results in a prolonged inhibitory synaptic potential which is dependent on metabolism and is selectively blocked by cooling and ouabain. In cells which have this synaptic potential, part of the resting membrane potential is also maintained by an electrogenic sodium pump. The same transmitter, acetylcholine, can independently stimulate both a chloride ion conductance and a sodium pump mechanism in the same follower cell by acting on two different postsynaptic receptors.     

Calcium current and activation of contraction in ventricular myocardial fibers

In thin bundles of dog ventricular myocardium, a slow inward current (distinct from the sodium inward current) could be recorded under voltageclamp conditions. This inward current was influenced by changes in external calcium concentration, but it was not dependent on external sodium concentration. Therefore, this current which contributes an appreciable amount of charge transfer during the plateau of the action potential, is carried by calcium ions. In sodium-free solution, the flow of calcium ions into the fiber is directly related to activation of contraction. In sodium-containing solution, however, calcium inward current serves primarily to fill up some intracellular stores from which calcium can be released by moderate depolarization.     

Strontium uptake in rats on alginate-supplemented diet

Rats were fed a basic diet supplemented with sodium alginate and with tracer amounts of strontium-85 and calcium-45. Absorption of strontium was always inhibited by the alginate to a greater extent than absorption of calcium. Discrimination against strontium was greatest in alginate containing a high proportion of guluronic acid.     

土壤中游离碳酸钙对土壤pH及酶活性的影响

游离碳酸钙是我国北方石灰性土壤的重要组成物质,密切影响着土壤的物理、化学、生物学性质以及土壤的环境学效应,但是将游离碳酸钙作为土壤重要组成物质而探讨其对土壤生物学特性尤其是对土壤酶活性的影响研究较少.通过研究探讨碳酸钙与土壤pH值之间的定量关系以及碳酸钙含量对土壤酶活性的影响,为进一步研究游离碳酸钙对土壤生物学性质及土壤环境效应的影响提供理论参考.采用实验室模拟培养及分析测试的方法进行试验.结果表明:土壤pH随游离碳酸钙含量的增加而增加,趋近于达到该试验条件下的最大值(pH=8.19),但并非呈直线相关,而是呈非线性相关关系.中性磷酸酶活性和转化酶随碳酸钙浓度的增加而降低,其最大降低幅度分别为0.402个活性单位和3.16个活性单位.碳酸钙含量与土壤pH值之间呈非线性相关关系.碳酸钙对土壤中性磷酸酶和转化酶活性产生极显著的抑制作用,对脲酶活性呈现低含量促进而高含量抑制的作用,而对过氧化氢酶则产生极显著的促进作用.