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1.
Calcium ion fulfills several criteria for identifying an intracellular messenger for light-adaptation in Limulus photoreceptors. Direct injection of Ca++ mimicks two aspects of light-adaptation; sequestration of intracellular calcium tends to prevent light-adaptation; and light induces an increase in intracellular Ca++ as demonstrated by two independent techniques.Presented at the EMBO-Workshop on Transduction Mechanism of Photoreceptors, Jülich, Germany, October 4–8, 1976 相似文献
2.
Dr. Robert D. Prusch Stella-Maris Goette Paula Haberman 《Cell and tissue research》1989,255(3):553-557
Summary Phagocytosis in Amoeba proteus can be induced with prostaglandins (PG). In addition, arachidonic acid (the fatty acid precursor to the PG-2 series) also induces phagocytosis. The induction of phagocytosis with arachidonic acid can be partially inhibited by the cyclooxygenase inhibitor indomethacin. Phagocytosis in the amoeba can also be induced with the chemotactic peptide N-formylmethionyl-leucylphenylalanine (NFMLP). The peptide presumably induces phagocytosis by interacting with receptors on the amoeba surface, which may initiate the release of arachidonic acid from membrane lipids. NFMLP-induced phagocytosis can also be partially inhibited by indomethacin. It is suggested that PG's or biochemically related substances may play a signal-coupling role during phagocytosis in the amoeba. 相似文献
3.
A study of the intracellular transport of calcium in rat heart 总被引:4,自引:0,他引:4
The distribution of in vivo injected 45Ca++ in the subcellular fractions of rat heart has been studied. Most of the radioactivity of the cell was found to be associated with the subcellular organelles; only a small fraction was recovered in the soluble phase. Mitochondria contained the greatest part of the total radioactivity associated with the subcellular organelles. After injection of 45Ca++ the specific activity of the mitochondrial calcium pool was several times higher than that of the calcium of the sarcoplasmic reticulum. Pentachlorophenol has been administered to rats to uncouple oxidative phosphorylation in heart mitochondria in vivo and its effect on the distribution of 45Ca++ in the heart studied. Under these conditions, it has been found that mitochondria contained much less 45Ca++ than the controls; this decrease was paralleled by an increase of the radioactivity associated with the microsomes and with the final supernatant. Experiments in which 45Ca++ was added to heart homogenates at 0° indicated that 45Ca++ also became bound to mitochondria and the other subcellular structures at 0°. However, PCP had no effect on the distribution of radioactivity among the subcellular fractions under these conditions. The results suggest that (1) energy-linked movements of Ca++ take place in mitochondria of the intact rat heart, (2) a part of the uptake of 45Ca++ by mitochondria does not depend on metabolism, and, (3) the movements of Ca++ in heart mitochondria in vivo are probably more active than those in the sarcoplasmic reticulum. 相似文献
4.
Summary Secretagogues of pancreatic enzyme secretion, the hormones pancreozymin, carbamylcholine, gastrin I, the octapeptide of pancreozymin, and caerulein as well as the Ca++-ionophore A 23187 stimulate45Ca efflux from isolated pancreatic cells. The nonsecretagogic hormones adrenaline, isoproterenol, secretin, as well as dibutyryl cyclic adenosine 3,5-monophosphate and dibutyryl cyclic guanosine 3,5-monophosphate have no effect on45Ca efflux. Atropine blocks the stimulatory effect of carbamylcholine on45Ca efflux completely, but not that of pancreozymin. A graphical analysis of the Ca++ efflux curves reveals at least three phases: a first phase, probably derived from Ca++ bound to the plasma membrane; a second phase, possibly representing Ca++ efflux from cytosol of the cells; and a third phase, probably from mitochondria or other cellular particles. The Ca++ efflux of all phases is stimulated by pancreozymin and carbamylcholine. Ca++ efflux is not significantly effected by the presence or absence of Ca++ in the incubation medium. Metabolic inhibitors of ATP production, Antimycin A and dinitrophenol, which inhibit Ca++ uptake into mitochondria, stimulate Ca++ efflux from the isolated cells remarkably, but inhibit the slow phase of Ca++ influx, indicating the role of mitochondria as an intracellular Ca++ compartment. Measurements of the45Ca++ influx at different Ca++ concentrations in the medium reveal saturation type kinetics, which are compatible with a carrier or channel model. The hormones mentioned above stimulate the rate of Ca++ translocation.The data suggest that secretagogues of pancreatic enzyme secretion act by increasing the rate of Ca++ transport most likely at the level of the cell membrane and that Ca++ exchange diffusion does not contribute to the45Ca++ fluxes.With the technical assistance of C. Hornung. 相似文献
5.
Masaru Sorimachi 《Journal of neurochemistry》1993,60(4):1236-1243
Abstract: Using fura-2 microfluorometry, I investigated the mechanism by which non-N-methyl-d -aspartate (NMDA) receptor agonists increase the cytosolic free calcium concentration ([Ca]in) in single cerebellar Purkinje cells isolated from 3–10-day-old rats. Kainate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate dose-dependently increased the cytosolic free Na+ concentration, which was measured using sodium-binding benzofuran isophthalate microfluorometry, confirming the Na+ influx through ion channels linked to non-NMDA receptors. The [Ca2+] increases induced by relatively lower concentrations of agonists were entirely dependent on external Ca2+ and were reduced by removal of external Na+ or by addition of a Ca2+ channel blocker, D600. The results indicate that the non-NMDA agonist–induced [Ca]in increase was due mainly to Ca2+ influx through voltage-dependent Ca2+ channels, which were activated by a massive Na+ influx. On the other hand, higher concentrations of agonists dose-dependently increased [Ca]in under conditions in which activation of voltage-dependent Ca2+ channels were blocked by a combination of Na+ removal with D600. These [Ca]in increases were Ca2+ dependent and little affected by adding a competitive NMDA antagonist. Non-NMDA agonists also stimulated influxes of Mn2+ and Co2+, both of which can be monitored by quenching fura-2 fluorescence under the same conditions. These results suggest that ion channels linked to non-NMDA receptors on immature Purkinje cells are permeable to Ca2+, Mn2+, and Co2+. 相似文献
6.
A simple, rapid method for determining depolarization-induced45Ca influx into synaptosomes is described. Synaptosomes which had been depolarized in the presence of45Ca were applied to a small column of Chelex-100 resin to separate free Ca2+ from that taken up by the tissue. Approximately 70% of the synaptosomal protein applied to the column was recovered in the initial eluate. The magnitude of45Ca uptake was dependent on the amount of Ca2+ in the incubation medium and on the KCl concentration. Calcium influx reached a plateau after 90 sec of incubation at 24°C. The Na+ channel activator veratridine also produced a substantial influx of45Ca, and this effect was blocked by tetrodotoxin. Thus, this ion exchange procedure makes it possible to measure depolarization-induced Ca2+ influx in synaptosomes without subjecting them to high vacuum or centrifugation pressures or to EGTA-containing solutions. 相似文献
7.
Stanislav D. Zakharov Xia Li Taya P. Red'ko Richard A. Dilley 《Journal of bioenergetics and biomembranes》1996,28(6):483-494
The 8-kDa subunit c of theE. coli F0 ATP-synthase proton channel was tested for Ca++ binding activity using a45Ca++ ligand blot assay after transferring the protein from SDS-PAGE gels onto polyvinyl difluoride membranes. The purified subunit c binds45Ca++ strongly with Ca++ binding properties very similar to those of the 8-kDa CF0 subunit III of choloroplast thylakoid membranes. The N-terminal f-Met carbonyl group seems necessary for Ca++ binding capacity, shown by loss of Ca++ binding following removal of the formyl group by mild acid treatment. The dicyclohexylcarbodiimide-reactive Asp-61 is not involved in the Ca++ binding, shown by Ca++ binding being retained in twoE. coli mutants, Asp61Asn and Asp61Gly. The Ca++ binding is pH dependent in both theE. coli and thylakoid 8-kDa proteins, being absent at pH 5.0 and rising to a maximum near pH 9.0. A treatment predicted to increase the Ca++ binding affinity to its F0 binding site (chlorpromazine photoaffinity attachment) caused an inhibition of ATP formation driven by a base-to-acid pH jump in whole cells. Inhibition was not observed when the Ca++ chelator EGTA was present with the cells during the chlorpromazine photoaffinity treatment. An apparent Ca++ binding constant on the site responsible for the UV plus chlorpromazine effect of near 80–100 nM was obtained using an EGTA-Ca++ buffer system to control free Ca++ concentration during the UV plus chlorpromazine treatment. The data are consistent with the notion that Ca++ bound to the periplasimic side of theE. coli F0 proton channel can block H+ entry into the channel. A similar effect occurs in thylakoid membranes, but the Ca++ binding site is on the lumen side of the thylakoid, where Ca++ binding can modulate acid-base jump ATP formation. The Ca++ binding to the F0 and CF0 complexes is consistent with a pH-dependent gating mechanism for control of H+ ion flux across the opening of the H+ channel.This work was supported in part by grants from the Department of Energy and the U.S. Department of Agriculture.On leave from the Institute of Soil Science and Photosynthesis, Russian Academy of Science, Pushchino, Russia. 相似文献
8.
H. Porzig 《The Journal of membrane biology》1970,2(1):324-340
Summary The passive Ca efflux from human red cell ghosts was studied in media of differing ion compositions and compared to the ATP-dependent Ca efflux. Cells were loaded with45Ca during reversible hemolysis, and the loss of radioactivity into the non-radioactive incubation medium was measured, usually for 3 hr at 37°C. Analysis of the efflux curves revealed that45Ca efflux followed the kinetics of a simple two-compartment system. In the concentration range between 0 and 1mm Ca in the external solution ([Ca++]
o
), the rate constant of passive Ca efflux (k min–1, fraction of45Ca lost per minute into the medium) increased from 0.00732 to 0.0150 min–1. There was no further increase at higher [Ca++]
o
. The relation between the rate constant of Ca efflux and [Ca++]
o
is thus characterized by saturation kinetics. The passive transfer system for Ca could also be activated by Sr. The alkali metal ions Na, K and Li did not seem to have any significant influence on passive Ca transfer. The passive Ca efflux was slightly inhibited by Mg and strongly inhibited by Pb. Under most experimental conditions, a fraction of 15 to 50% of the intracellular Ca seemed to be inexchangeable. The inexchangeable fraction decreased with increasing [Ca++]
o
and increased with increasing [Ca++]
i
. It was not influenced by alkali metal ions, CN or Pb, but it could be completely removed from the cells by the addition of 0.1mm Mersalyl to the incubation medium or by hemolysis with addition of a detergent. The active ATP-dependent Ca transport differed characteristically from passive transfer; the rate constant decreased with increasing [Ca++]
o
, and the inexchangeable Ca fraction increased with increasing [Ca++]
o
. The experimental results suggest that there exists a carrier-mediated Ca–Ca exchange diffusion in the erythrocyte membrane and that only a fraction of the ghost cell population participates in the Ca exchange diffusion. 相似文献
9.
The Initiation of Spike Potential in Barnacle Muscle Fibers under Low Intracellular Ca++ 总被引:11,自引:17,他引:11
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Electrical properties of the muscle fiber membrane were studied in the barnacle, Balanus nubilus Darw. by using intracellular electrode techniques. A depolarization of the membrane does not usually produce an all-or-none spike potential in the normal muscle fiber even though a mechanical response is elicited. The intracellular injection of Ca++-binding agents (K2SO4 and K salt of EDTA solution, K3 citrate solution, etc.) renders the fiber capable of initiating all-or-none spikes. The overshoot of such a spike potential increases with increasing external Ca concentration, the increment for a tenfold increase in Ca concentration being about 29 mv. The threshold membrane potential for the spike and also for the K conductance increase shifts to more positive membrane potentials with increasing [Ca++]out. The removal of Na ions from the external medium does not change the configuration of the spike potential. In the absence of Ca++ in the external medium, the spike potential is restored by Ba++ and Sr++ but not by Mg++. The overshoot of the spike potential increases with increasing [Ba++]out or [Sr++]out. The Ca influx through the membrane of the fiber treated with K2SO4 and EDTA was examined with Ca45. The influx was 14 pmol per sec. per cm2 for the resting membrane and 35 to 85 pmol per cm2 for one spike. From these results it is concluded that the spike potential of the barnacle muscle fiber results from the permeability increase of the membrane to Ca++ (Ba++ or Sr++). 相似文献
10.
Summary Binding of the tripeptide n-formylmethionyl-leucylphenylalanine (NFMLP) to phagocytic receptors on the surface of Amoeba proteus was examined. Peptide-binding is reversible and demonstrates saturation kinetics. The receptors for phagocytosis are internalized by a temperature-sensitive process with indications that the receptors are recycled. The amoeba is capable of down-regulating its receptors for phagocytosis in response to constant external peptide levels, and also increasing the number of surface receptors in response to food deprivation. On the basis of competition studies, there is evidence that Amoeba proteus has separate surface receptors for both pinocytosis and phagocytosis. 相似文献
11.
Summary Different methods were used to demonstrate the existence of Ca++-binding sites (Ca++-bs) at the plasma membrane ofAmoeba proteus. In pinocytoting animals the number (indicated by the average distanced in nm) and size (average longitudinal axiss in nm) of Ca++-bs at the cytoplasmic surface of the cell membrane were significantly increased (d=162±15;n=41 ands=93±5;n=47) in comparison to controls (d=208 ±21;n=37 ands=59±8;n=45). The ratio of P: Ca obtained by X-ray microanalysis was in the range of 1.5. The differences observed in the two experimental groups of amoebae are explained by conformational changes in the molecular structure and an increased Ca++-permeability of the plasma membrane during induced pinocytosis.Microplasmodia of the acellular slime moldPhysarum polycephalum investigated for comparison were found to have no Ca++-bs at the interior cell surface. 相似文献
12.
Pentobarbital depression of potassium-stimulated 45Ca++ influx was examined in synaptosomes prepared from animal species and strains with reported differences in their sensitivity to pentobarbital sedation. Synaptosomes were isolated from New Zealand, white rabbits, Sprague-Dawley rats, C57/6J mice and DBA/2J mice. Synaptosomes isolated from the various groups were challenged with concentrations of 0.15, 0.30, 0.45 and 0.60 mM pentobarbital in incubation medium and compared with synaptosomes in incubation medium alone to assess the degree of depression of 45Ca++ influx. The results show that pentobarbital significantly depresses 45Ca++ influx to approximately the same extent in all animal groups at concentrations of 0.30 mM and higher. It is concluded that reported differences in pentobarbital sedative sensitivity between these animal groups does not involve differences in calcium influx. Further, the data show that inhibition of 45Ca++ influx by pentobarbital is generalizable across several animal strains and species and suggest, as we have previously reported, that inhibition of calcium influx across the presynaptic nerve ending may provide a mechanism through which the barbiturates produce sedation. 相似文献
13.
Klaus Lange 《Journal of cellular physiology》1999,180(1):19-34
Proceeding from the recent finding that the main components of the Ca++ signal pathway are located in small membrane protrusions on the surface of differentiated cells, called microvilli, a novel concept of cellular Ca++ signaling was developed. The main features of this concept can be summarized as follows: Microvilli are formed on the cell surface of differentiating or resting cells from exocytic membrane domains, growing out from the cell surface by elongation of an internal bundle of actin filaments. The microvillar tip membranes contain all functional important proteins synthesized such as ion channels and transporters for energy-providing substrates and structural components, which are, in rapidly growing undifferentiated cells, distributed over the whole cell surface by lateral diffusion. The microvillar shaft structure, a bundle of actin filaments, forms a dense cytoskeletal matrix tightly covered by the microvillar lipid membrane and represents an effective diffusion barrier separating the microvillar tip compartment (entrance compartment) from the cytoplasm. This diffusion barrier prevents the passage of low molecular components such as Ca++ glucose and other relevant substrates from the entrance compartment into the cytoplasm. The effectiveness of the actin-based diffusion barrier is modulated by various signal pathways and effectors, most importantly, by the actin-depolymerizing/reorganizing activity of the phospholipase C (PLC)-coupled Ca++ signaling. Moreover, the microvillar bundle of actin filaments plays a dual role in Ca++ signaling. It combines the function of a diffusion barrier, preventing Ca++ influx into the resting cell, with that of a high-affinity, ATP-dependent, and IP3-sensitive Ca++ store. Activation of Ca++ signaling via PLC-coupled receptors simultaneously empties Ca++ stores and activates the influx of external Ca++. The presented concept of Ca++ signaling is compatible with all established data on Ca++ signaling. Properties of Ca++ signaling, that could not be reconciled with the basic principles of the current hypothesis, are intrinsic properties of the new concept. Quantal Ca++ release, Ca++-induced Ca++ release (CICR), the coupling phenomen between the filling state of the Ca++ store and the activity of the Ca++ influx pathway, as well as the various yet unexplained complex kinetics of Ca++ uptake and release can be explained on a common mechanistic basis. J. Cell. Physiol. 180:19–34, 1999. © 1999 Wiley-Liss, Inc. 相似文献
14.
de Andrade Antero S.R. dos Santos Raquel G. Nicoli Jacques R. Neves Maria J. 《World journal of microbiology & biotechnology》2000,16(7):691-694
Lyophilized cells of the non-pathogenic yeast Saccharomyces boulardii are used in many countries for the treatment of several types of diarrhoea and other gastrointestinal diseases. Although
the cells must be viable, their mechanism of action is unknown. The disaccharide trehalose is a protectant against several
forms of environmental stress in yeast and is involved in maintaining cell viability. There is no information on the enzymes
involved in degradation of trehalose in S. boulardii. The aim of the present study was to characterize trehalase activity in this yeast. Cells of S. boulardii grown in glucose exhibited neutral trehalase activity only in the exponential phase. Acidic trehalase was not detected in
glucose medium. Cells grown in trehalose exhibited acid and neutral trehalase activities at all growth stages, particularly
in the exponential phase. The optimum pH and temperature values for neutral trehalase activity were determined as 6.5 and
30 °C respectively, the half-life being approximately 3 min at 45 °C. The relative molecular mass of neutral trehalase is
80 kDa and the K
m 6.4 mM (±0.6). Neutral trehalase activity at pH 6.5 was weakly inhibited by 5 mM EDTA and strongly inhibited by ATP, as well
as the divalent ions Cu++, Fe++ and Zn++. Enzyme activity was stimulated by Mg++ and Ca++ only in the absence of cAMP. The presence of cAMP with no ion additions increased activity by 40%.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
15.
Primary cultures of bone cells and skin fibroblasts were examined for their Ca++ content, intracellular distribution and Ca++ fluxes. Kinetic analysis of 45Ca++ efflux curves indicated the presence of three exchangeable Ca++ compartments which turned over at different rates: a “very fast turnover” (S1), a “fast turnover” (S2), and a “slow turnover” Ca++ pool (S3). S1 was taken to represent extracellular membrane-bound Ca++, S2 represented cytosolic Ca++, and S3 was taken to represent Ca++ sequestered in some intracellular organelles, probably the mitochondria. Bone cells contained about twice the amount of Ca++ as compared with cultured fibroblasts. Most of this extra Ca++ was localized in the “slow turnover” intracellular Ca++ pool (S3). Serum activation caused the following changes in the amount, distribution, and fluxes of Ca++: (1) In both types of cells serum caused an increase in the amount of Ca++ in the “very fast turnover” Ca++ pool, and an increase in the rate constant of 45Ca++ efflux from this pool, indicating a decrease in the strength of Ca++ binding to ligands on cell membranes. (2) In fibroblasts, serum activation also caused a marked decrease in the content of Ca++ in the “slow turnover” Ca++ pool (S3), an increase in the rates of Ca++ efflux from the cells to the medium, and from S3 to S2, as well as a decrease in the rate of influx into S3. (3) In bone cells the amount of Ca++ in S3 remained high in “serum activated” cells, the rate of efflux from S3 to S2 increased, and the rate of influx into S3 also increased. The rate of efflux from the cells to the medium did not change. The results suggest specific properties of bone cells with regard to cell Ca++ presumably connected with their differentiation. Following serum activation we investigated the time course of changes in the amount of exchangeable Ca++ in bone cells and fibroblasts, in parallel with measurements of 3H-thymidine incorporation and cell numbers. Serum activation caused a rapid decrease in the content of cell Ca++ which was followed by a biphasic increase lasting until cell division. 相似文献
16.
Effects of calcium and salinity on the growth rate of Ephydatia fluviatilis (Porifera: Spongillidae)
The freshwater sponge, Ephydatia fluviatilis (Porifera: Spongillidae), was maintained in a continuous-flow laboratory culture system under several conditions of calcium ion (Ca++) concentration and salinity. Experimental results suggest that sponge growth rate increases with increasing Ca++ concentration, that sponge growth rate decreases with increasing salinity, and that the negative effect of higher salinity can be overcome by increasing Ca++ concentration. The experimental results correlate well with field observations on the effects of salinity and Ca++ on the distribution of E. fluviatilis. 相似文献
17.
D E Woolley 《Journal of cellular physiology》1970,76(2):185-190
An actomyosin-like protein has been extracted from amoebae of Dictyostelium discoideum, V-12. The purified protein exhibited a reversible change in viscosity upon addition of ATP, indicating an ATP sensitivity of 75–85% and a specific viscosity of 0.1. At low ionic strength in the presence of Mg++ and ATP the amoeba protein displayed the phenomenon of superprecipitation. The protein extract was found to be an adenosinetriphosphatase (ATP'ase) hydrolyzing ATP to ADP and inorganic phosphate. Both Mg++ and Ca++ at low ionic strength accelerated the ATP ase activity whereas at high ionic strength only Ca++ stimulated ATP hydrolysis. The ATP'ase activity was inhibited by ethylene-diamine-tetraacetic-acid, Mersayl and p-chloromercuribenzoate. The physico-chemical and enzymatic properties of the extracted amoeba protein are qualitatively comparable to those of muscle actomyosin, and very similar in quantitative properties to smooth muscle actomyosin and the actomyosin-like proteins of blood platelets, leucocytes and slime mold plasmodia. The significance of the presence of this actomyosin-like protein in Dictyostelium amoebae is discussed in relation to amoeboid form and movement. 相似文献
18.
E. A. C. MacRobbie 《Planta》1989,178(2):231-241
The influx of 45Ca into isolated guard cells of Commelina communis L. has been measured, using short uptake times, and washing in ice-cold La3+-containing solutions to remove extracellular tracer after the loading period. Over 0.5–4 min the uptake was linear with time, through the origin. Over 20–200M external Ca2+ the influx measured with 10–20 mM external KCl was in the range 0.3–2.3 pmol·cm-2·s-1 (on the basis of estimated guard-cell area); with only 1 mM KCl externally the 45Ca influx was significantly reduced, in the range 0.3–1.1 pmol·cm-2·s-1 for external Ca2+ of 50–100 M. The results indicate that the Ca-channel is voltage-sensitive, opening with depolarisation. No consistent effect of the addition of abscisic acid could be found. In different experiments, on the addition of 0.1 mM abscisic acid the Ca2+ influx was sometimes stimulated by 28–79%, was sometimes unaffected, and was sometimes inhibited by 16–29%. The results rule out a long-lasting stimulation of 45Ca influx by ABA, but they do not rule out a transient stimulation followed by inhibition, perphaps as a consequence of down-regulation of Ca2+ influx by increasing cytoplasmic Ca2+. The hypothesis that ABA may act via an action on Ca2+ influx, increasing cytoplasmic Ca2+, with consequent effects on voltage-dependent and Ca2+-dependent ion channels in both plasmalemma and tonoplast, is neither proved nor disproved by these results.Abbreviations ABA
abscisic acid
- Cao, Ko
external Ca and K concentrations 相似文献
19.
Rapid plant movements triggered by action potentials 总被引:4,自引:0,他引:4
Takao Sibaoka 《Journal of plant research》1991,104(1):73-95
Rapid bendings of the pulvinus inMimosa pudica, of the trap lobes inDionaea muscipula andAldrovanda vesiculosa, and of the tentacle in Drosera are triggered by action potentials in their motor cells. The action potential ofMimosa may be a C1−-spike, and that ofDionaea andAldrovanda may be a Ca2+-spike. Propagation of action potentials in the petiole or motor organ is thought to be electrotonie, cell-to-cell, transmission.
The Ca 2+ release from unidentified organelles in the pulvinus or the Ca2+ influx of the cells in the trap with the action current and activation of contractile fibrillar network having ATPase activity
in the cytoplasm must be involved in the rapid bending. Contractions of fibrils may open pores in the membrane of the motor
cells upon activation. Outward bulk flow of the vacuolar sap through these pores, due to the pressure inside the cell, must
result in turgor loss of the motor cells and then the bending of the organ. 相似文献
20.
The tissue/medium distribution of the nonmetabolized glucose analog [14C]-3-0-methyl-D-glucose was measured in pigeon erythrocytes and related to changes in 45Ca uptake and efflux, total calcium content and ATP levels. Sugar transport was not affected by changes in external Ca2+. However, both sugar and 45Ca influx were increased by the Ca-ionophore A23187. In the absence of external Ca2+, the ionophore caused a delayed increase in sugar transport and net loss of calcium, probably through releasing Ca2+ from internal storage sites into the cytoplasm. Increasing internal Na+ through Na+ pump inhibition or using the sodium ionophore monensin did not alter influx of sugar or 45Ca, indicating Na+-Ca2+ exchange was absent in these cells. The results are consistent with A23187 causing increased Ca2+ influx or release from mitochondrial storage and the resulting rise in cytoplasmic Ca2+ stimulating hexose transport. Experiments with low Mg++ and high K+ media and measurements of ATP levels exclude alternative explanations for the action of A23187. We conclude that sugar transport regulation in avian erythrocytes is Ca2+-dependent and resembles that in muscle in its basic mechanism. It differs in the response to some modulating agents, largely because of a different pattern of Ca2+ fluxes in these cells. 相似文献