共查询到20条相似文献,搜索用时 52 毫秒
1.
H. Gesser O. Poupa 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1981,143(2):245-251
Summary The effect of acidosis on the myocardial Ca2+ distribution was examined at 15°C in ventricular strips of the flounder (Platichthys flesus) and at 30°C in atrial strips of the rat (Rattus norvegicus).Lowering the Ringer pH from 7.6 to 6.9 by increasing its CO2 (flounder 2% to 12%, rat 4% to 14%), resulted in an elevated Ca2+ efflux in resting strips as well as in strips stimulated (12/min) to contraction. A decrease in pH of the Ringer used for the flounder myocardium by a lowering of bicarbonate (30 mM to 5 mM) also resulted in an elevation of the Ca2+ efflux, but the effect was smaller than that produced by an increased CO2.With 11 mM Ca2+ and 10 mM EGTA added to the Ringer to reduce the amount of45Ca2+ bound to extracellular sites, an increased CO2 with a concomitant drop in Ringer pH resulted in an increased Ca2+ efflux in both myocardia. The Ca2+ efflux was only marginally elevated in the flounder myocardium and unchanged in that of rat when the same drop in Ringer pH was produced with a lowering in bicarbonate.In a nominally Ca2+-free Ringer with 0.1 mM EGTA the45Ca2+ efflux was stimulated for both myocardia by an increase in CO2.The flounder myocardium was exposed to high CO2 in a nominally Na+, Ca2+-free Ringer and again the45Ca2+ efflux increased. After a return to Na, Ca and low CO2 in the Ringer, a higher efflux persisted in the strips being subjected to a high CO2 than in the controls.The Ca2+ uptake rate was about the same at high and low CO2 for both myocardia.Based on these results the measured increase in Ca efflux following an increase in CO2 or a decrease in bicarbonate probably results from an elevated cytoplasmatic Ca2+ activity. It seems unlikely that an increased uptake rate of Ca2+ or a direct stimulation of Ca2+ transporting mechanisms in the cell membrane are responsible for the change. 相似文献
2.
W. M. MacKenzie S. F. Perry 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1997,167(1):52-60
Whole body calcium influx, branchial calcium efflux, and renal Ca2+ excretion were measured in rainbow trout (Oncorhynchus mykiss) exposed to hypercapnia. These experiments were performed to assess the potential impact on Ca2+ balance of the changes in gill morphology known to accompany respiratory acidosis in this species. After 48 h of hypercapnia,
gill filamental chloride cell fractional area was significantly reduced. Despite this reduction and the presumed involvement
of the chloride cell in calcium influx, whole body calcium influx was increased after 12 h of hypercapnia and remained elevated
for 48 h. Branchial calcium efflux was unaltered during hypercapnia exposure, whereas renal Ca2+ excretion was elevated over preflux values only at 6 h of hypercapnia. Measurement of the kinetics of whole body calcium
influx after 48 h of hypercapnia revealed a significant increase in the maximal uptake rate of Ca2+, yet the affinity constant of Ca2+ uptake was unaffected. Measurements of high-affinity Ca2+ -ATPase activities and ATP-dependent Ca2+ transport of gill basolateral membrane vesicles revealed that the ATP-dependent Ca2+ extrusion mechanism of the gills was not affected by hypercapnia. The results of the present study clearly show that the
reduced chloride cell surface area that accompanies hypercapnia in trout does not impair calcium homeostasis. Although adjustments
to the basolateral membrane high affinity Ca2+ transporter do not appear to play a role, the mechanism(s) underlying the maintenance of calcium homeostasis under hypercapnic
conditions are unresolved.
Accepted: 1 July 1996 相似文献
3.
Effect of cytoplasmic acidification on the membrane potential of T-lymphocytes: Role of trace metals
Summary The effect of lowering intracellular pH on the membrane potential (E
m
) of rat thymic lymphocytes was studied using the potential-sensitive dyebis-oxonol. Cells were acid loaded by addition of the electroneutral K+/H+ exchanging ionophore nigericin. Acidification to pH 6.3 in Na+-free solution resulted in a biphasic change inE
m
: an early transient hyperpolarization followed by a sustained depolarization. These changes were associated with a rise in cytosolic free Ca2+ ([Ca2+]
i
). The hyperpolarization was eliminated when the change in [Ca2+]
i
was prevented using BAPTA, an intracellular Ca2+ chelator. Moreover, a similar hyperpolarization was elicited by elevation of [Ca2+]
i
at physiological pH
i
using ionomycin, suggesting involvement of Ca2+-activated K+ channels. In contrast, the depolarization phase could not be mimicked by raising [Ca2+]
i
with ionomycin. However, intracellular BAPTA effectively inhibited the acidificationinduced depolarization. Inhibition was also obtained by extracellular addition of EGTA or dithiothreitol, even when the external free Ca2+ concentration remained unaltered. These observations suggested a possible role of contaminating trace metals. Cytosolic acidification is envisaged to induce intracellular accumulation of one or more trace metals, which induces the observed changes inE
m
. Accordingly, similar changes inE
m
can be induced without acidification by the addition of small amounts of Cu2+ to the medium. The ionic basis of theE
m
changes induced by acidification and the significance of these observations are discussed. 相似文献
4.
Erik Allman Korrie Waters Sarah Ackroyd Keith Nehrke 《The Journal of biological chemistry》2013,288(8):5886-5895
Membrane proton transporters contribute to pH homeostasis but have also been shown to transmit information between cells in close proximity through regulated proton secretion. For example, the nematode intestinal Na+/H+ exchanger NHX-7 causes adjacent muscle cells to contract by transiently acidifying the extracellular space between the intestine and muscle. NHX-7 operates during a Ca2+-dependent rhythmic behavior and contains several conserved motifs for regulation by Ca2+ input, including motifs for calmodulin and phosphatidylinositol 4,5-bisphosphate binding, protein kinase C- and calmodulin-dependent protein kinase type II phosphorylation, and a binding site for calcineurin homologous protein. Here, we tested the idea that Ca2+ input differentiates proton signaling from pH housekeeping activity. Each of these motifs was mutated, and their contribution to NHX-7 function was assessed. These functions included pH recovery from acidification in cells in culture expressing recombinant NHX-7, extracellular acidification measured during behavior in live moving worms, and muscle contraction strength as a result of this acidification. Our data suggest that multiple levels of Ca2+ input regulate NHX-7, whose transport capacity normally exceeds the minimum necessary to cause muscle contraction. Furthermore, extracellular acidification limits NHX-7 proton transport through feedback inhibition, likely to prevent metabolic acidosis from occurring. Our findings are consistent with an integrated network whereby both Ca2+ and pH contribute to proton signaling. Finally, our results obtained by expressing rat NHE1 in Caenorhabditis elegans suggest that a conserved mechanism of regulation may contribute to cell-cell communication or proton signaling by Na+/H+ exchangers in mammals. 相似文献
5.
6.
Abstract: Modes of Ca2+ activation by bradykinin, serotonin, and ATP and the possible receptor cross-talk were investigated in mouse neuroblastoma × rat glioma hybrid cells (108CC15) by monitoring fura-2 fluorescence in single cells. A transient rise of cytosolic Ca2+ activity was induced by short pulses of the hormones. Brief exposure of cells to ionomycin, which depletes intracellular Ca2+ stores, reduced the size of subsequent responses to bradykinin or ATP, but not to serotonin. Superfusion of the cells with Ca2+-free medium abolished the Ca2+ response to serotonin, whereas the responses to bradykinin and to ATP were only slightly reduced. This indicates that ATP, like bradykinin, Induces the release of Ca2+ from intracellular stores. Serotonin, in contrast, activates Ca2+ entry from the extracellular space. To investigate whether ATP releases Ca2+ from the same stores as bradykinin, we examined the interaction of the hormones by applying them consecutively. When ATP was applied after bradykinin, the nucleotide did not evoke any response, irrespective of the presence or absence of extracellular Ca2+. The application of ATP before that of bradykinin reduced the size of a following bradykinin-induced Ca2+ response in Ca2+-free medium, but not in Ca2+-containing medium. This suggests that bradykinin may interact with the ATP-activated mechanism by cross-desensitization. Possibly, bradykinin receptors are coupled to additional Ca2+ stores not accessible to ATP that are refilled by extracellular Ca2+. Cyclic AMP and cyclic GMP apparently do not affect the Ca2+ responses to bradykinin and serotonin, as shown by the lack of influence of preincubation of the cells with forskolin or sodium nitroprusside. 相似文献
7.
Farzaneh Ketabchi Hossein A Ghofrani Ralph T Schermuly Werner Seeger Friedrich Grimminger Bakytbek Egemnazarov S Mostafa Shid-Moosavi Gholam A Dehghani Norbert Weissmann Natascha Sommer 《Respiratory research》2012,13(1):1-16
Background
Acute respiratory disorders may lead to sustained alveolar hypoxia with hypercapnia resulting in impaired pulmonary gas exchange. Hypoxic pulmonary vasoconstriction (HPV) optimizes gas exchange during local acute (0-30 min), as well as sustained (> 30 min) hypoxia by matching blood perfusion to alveolar ventilation. Hypercapnia with acidosis improves pulmonary gas exchange in repetitive conditions of acute hypoxia by potentiating HPV and preventing pulmonary endothelial dysfunction. This study investigated, if the beneficial effects of hypercapnia with acidosis are preserved during sustained hypoxia as it occurs, e.g in permissive hypercapnic ventilation in intensive care units. Furthermore, the effects of NO synthase inhibitors under such conditions were examined.Method
We employed isolated perfused and ventilated rabbit lungs to determine the influence of hypercapnia with or without acidosis (pH corrected with sodium bicarbonate), and inhibitors of endothelial as well as inducible NO synthase on acute or sustained HPV (180 min) and endothelial permeability.Results
In hypercapnic acidosis, HPV was intensified in sustained hypoxia, in contrast to hypercapnia without acidosis when HPV was amplified during both phases. L-NG-Nitroarginine (L-NNA), a non-selective NO synthase inhibitor, enhanced acute as well as sustained HPV under all conditions, however, the amplification of sustained HPV induced by hypercapnia with or without acidosis compared to normocapnia disappeared. In contrast 1400 W, a selective inhibitor of inducible NO synthase (iNOS), decreased HPV in normocapnia and hypercapnia without acidosis at late time points of sustained HPV and selectively reversed the amplification of sustained HPV during hypercapnia without acidosis. Hypoxic hypercapnia without acidosis increased capillary filtration coefficient (Kfc). This increase disappeared after administration of 1400 W.Conclusion
Hypercapnia with and without acidosis increased HPV during conditions of sustained hypoxia. The increase of sustained HPV and endothelial permeability in hypoxic hypercapnia without acidosis was iNOS dependent. 相似文献8.
Yuji Shono Masahiro Kamouchi Takanari Kitazono Junya Kuroda Kuniyuki Nakamura Noriko Hagiwara Hiroaki Ooboshi Setsuro Ibayashi Mitsuo Iida 《Cellular and molecular neurobiology》2010,30(3):453-460
Brain hypoxia or ischemia causes acidosis and the intracellular accumulation of Ca2+ in neuron. The aims of the present study were to elucidate the interaction between intracellular pH and Ca2+ during transient acidosis and its effects on the viability of neuronal and glial cells. Intracellular Ca2+ and pH were measured using the fluorescence of fura-2 and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl
ester in neuroblastoma (IMR-32), glioblastoma (T98G), and astrocytoma (CCF-STTG1) cell lines. The administration of 5 mM propionate
caused intracellular acidification in IMR-32 and T98G cells but not in CCF-STTG1 cells. After the removal of propionate, the
intracellular pH recovered to the resting level. The intracellular Ca2+ transiently increased upon the removal of propionate in IMR-32 and T98G cells but not in CCF-STTG1 cells. The transient Ca2+ increase caused by the withdrawal of intracellular acidification was abolished by the removal of external Ca2+, diminished by a reduction of external Na+, and inhibited by benzamil. Transient acidosis caused cell death, whereas the cells were more viable in the absence of external
Ca2+. Benzamil alleviated cell death caused by transient acidosis in IMR-32 and T98G cells but not in CCF-STTG1 cells. These results
suggest that recovery from intracellular acidosis causes a transient increase in cytosolic Ca2+ due to reversal of Ca2+ transport via Na+/Ca2+ exchanger coactivated with Na+/H+ exchanger, which can cause cell death. 相似文献
9.
Calcium-calmodulin signalling is involved in light-induced acidification by epidermal leaf cells of pea, Pisum sativum L. 总被引:2,自引:0,他引:2
Elzenga J. Theo M.; Staal Marten; Prins Hidde B.A. 《Journal of experimental botany》1997,48(12):2055-2061
Pathways of signal transduction of red and blue light-dependentacidification by leaf epidermal cells were studied using epidermalstrips of the Argenteum mutant of Pisum sativum. In these preparationsthe contribution of guard cells to the acidification is minimal.The hydroxypyridine nifedipine, a Ca2+-channel blocker, partlyinhibited the response to both blue and red light, while thephenylalkylamine, verapamil, a Ca2+-channel blocker that hasbeen shown in plant cells also to block K+-channels, causednearly complete inhibition. The Ca2+-channel activator S()BayK 8644 induced acidification when added in the dark and diminishedthe light-induced lowering of the extracellular pH. The Ca2+-ionophores,ionomycin and A23187
[GenBank]
, also reduced the light response. Furthermore,the light-induced acidification was inhibited by the calmodulinantagonists W-7 and trifluoperazine, but not by W-5. These calmodulininhibitors completely inhibited the red light-induced acidification,but inhibited the response to blue light by only 6070%.In general, inhibition by compounds affecting Ca-calmodulinsignalling was always stronger on the red light response thanthat on the blue light response (with the exception of verapamilthat blocked both the red and blue light responses equally well).This differential effect on red and blue light-induced responsesindicates a role for Ca2+-CaM signalling in both the red andblue light responses, while a second process, independent ofCa2+ is activated by blue light. Key words: Signal transduction, light-induced acidification, epidermal cells, pea 相似文献
10.
Characterization of Low pH-induced Catecholamine Secretion in the Rat Adrenal Medulla 总被引:1,自引:0,他引:1
Abstract: Catecholamine (CA) secretion was evoked when the isolated rat adrenal gland was perfused with HEPES-buffered Krebs solution acidified by the addition of HCI or by gassing with 95% O2/5% CO2. The secretion was detectable at pH 7.0 and increased with decreasing pH until at ~6.4. The low pH-induced CA secretion consisted of two phases, an initial transient response followed by a sustained phase. An intracellular Ca2+ antagonist, 3,4,5-trimethoxybenzoic acid 8-(N,N-diethylamino)octyl ester, selectively inhibited the initial phase of secretion. Both of the responses were resistant to nifedipine, a blocker of voltage-gated Ca2+ channel, but were completely inhibited in Ca2+-free (1 mM EGTA containing) solution. Adrenaline was an exclusive component in CAs released by low pH. The time course and extent of intracellular acidification caused either by low pH in the external medium or by the offset of a transitory NH4CI application had no correlation with those of the secretory responses in the corresponding period. These results suggest that extracellular acidification preferentially activates adrenaline secretive cells to evoke CA secretion and that this low pH-induced CA secretion may be mediated by dihydropyridine-insensitive Ca2+ influx. Furthermore, the initial transient phase of the low pH-induced CA secretion might be caused by a Ca2+ release from intracellular stores, which is also induced by the Ca2+ influx. 相似文献
11.
《Cell calcium》2019
Alterations in the (bio)chemical and physical microenvironment of cells accompany and often promote disease formation and progression. This is particularly well established for solid cancers, which are typically stiffer than the healthy tissue in which they arise, and often display profound acidification of their interstitial fluid. Cell surface receptors can sense changes in the mechanical and (bio)chemical properties of the surrounding extracellular matrix and fluid, and signalling through these receptors is thought to play a key role in disease development and advancement. This review will look at ion channels and G protein coupled receptors that are activated by mechanical cues and extracellular acidosis, and stimulation of which results in increases in intracellular Ca2+ concentrations. Cellular Ca2+ levels are dysregulated in cancer as well as cancer-associated cells, and mechano- and proton-sensing proteins likely contribute to these aberrant intracellular Ca2+ signals, making them attractive targets for therapeutic intervention. 相似文献
12.
Abstract: The ability of various stimuli to convert Ca2+/calmodulin-dependent protein kinase II (CaMKII) into a Ca2+-independent (autonomous) form was examined in cultured embryonic rat hippocampal pyramidal neurons. The most effective stimulation by far was observed when cells were equilibrated in buffer containing low extracellular [Ca2+] ([Ca2+]o) (~50 nM) and then shifted to normal [Ca2+]o (~1.26 mM) by addition of CaCl2 (referred to as “Ca2+ stimulation”). Virtually complete (>90%) conversion of the kinase to the autonomous form occurred within 30–50 s, with a return to baseline within 5 min. By contrast, depolarization of cells with high [K+] or treatment with glutamate or a Ca2+ ionophore caused insignificant increases (<10%) in levels of the autonomous form. The Ca2+-stimulated increase in CaMKII autonomy coincided with a two- to threefold increase in kinase subunit phosphorylation. In the first 40 s of Ca2+ stimulation, 32P incorporation into the immunoprecipitated subunits of CaMKII occurred exclusively on threonine residues, including Thr286Thr287 of the α/β subunits. Longer incubation of cells resulted in a decline of phosphothreonine content, whereas levels of phosphoserine-containing peptides showed a significant increase. The activation of CaMKII by Ca2+ stimulation was accompanied by only a small rise in intracellular [Ca2+]. Inhibitor studies showed that Na+-dependent action potentials and Ca2+ influx through glutamate receptors or voltage-sensitive Ca2+ channels did not contribute to the activation. Moreover, CaMKII was not activated by extracellular addition of other cations, including Mn2+, Mg2+, Co2+, or Gd3+. Although the mechanism of Ca2+ stimulation is presently unclear, it may involve either activation of extracellular calcium receptors or capacitative calcium entry. The dramatic rise in CaMKII autonomy and the Ca2+ selectivity of the response suggest a direct and specific relationship between [Ca2+]o and the state of activation of the kinase in intact neurons. 相似文献
13.
Both oxalate-supported Ca2+ uptake and Ca2+-stimulated ATPase activity of the sarcoplasmic reticulum are sensitive to the pH of the assay medium. Ca2+ uptake is optimal at relatively acidic pH (6.2–6.6); whereas, Ca2+-stimulated ATPase activity is optimal at a more alkaline pH (7.4–8.0). Following the addition of ATP, Ca2+ uptake demonstrates a time-dependent resistance to the inhibition by an alkaline pH. Once the linear phase of Ca2+ uptake is reached, alkalinization thereafter does not alter the rate established at the acidic pH. A similar time-dependent resistance is observed to the inhibition of Ca2+ uptake by the cation ionophore, X537A. In contrast, acidification of the alkaline medium after Ca2+ uptake is initiated by ATP has no such resistance to change. Acidification results in a prompt acceleration of the rate of Ca2+ uptake identical to that observed under control conditions at the acidic pH. Ca2+-stimulated ATPase activity, however, increases with alkalinization and decreased with acidification, regardless of time, in a manner expected from the rates observed under conditions when the pH is constant from the time of ATP addition. The results suggest that there is a time-dependent, pH-sensitive factor of oxalate-supported Ca2+ uptake. This factor can be activated by acidification at any time after ATP addition and, thus, does not represent a destruction of membrane function. In contrast, Ca2+-stimulated ATPase activity demonstrates no time-dependent resistance to pH change. 相似文献
14.
Péter M Varga Z Hajdu P Gáspár R Damjanovich S Horjales E Possani LD Panyi G 《The Journal of membrane biology》2001,179(1):13-25
We investigated the cytosolic free Ca2+ concentration ([Ca2+]i) of leech Retzius neurons in situ while varying the extracellular and intracellular pH as well as the extracellular ionic
strength. Changing these parameters had no significant effect on [Ca2+]i when the membrane potential of the cells was close to its resting value. However, when the cells were depolarized by raising
the extracellular K+ concentration or by applying the glutamatergic agonist kainate, extracellular pH and ionic strength markedly affected [Ca2+]i, whereas intracellular pH changes appeared to have virtually no effect. An extracellular acidification decreased [Ca2+]i, while alkalinization or reduction of the ionic strength increased it. Correspondingly, [Ca2+]i also increased when the kainate-induced extracellular acidification was reduced by raising the pH-buffering capacity. At
low extracellular pH, the membrane potential to which the cells must be depolarized to evoke a detectable [Ca2+]i increase was shifted to more positive values, and it moved to more negative values at high pH. We conclude that in leech
Retzius neurons extracellular pH, but not intracellular pH, affects [Ca2+]i by modulating Ca2+ influx through voltage-dependent Ca2+ channels. The results suggest that this modulation is mediated primarily by shifts in the surface potential at the extracellular
side of the plasma membrane.
Received: 23 January 2001/Revised: 15 June 2001 相似文献
15.
Hong Shan Zhang Thomas V. McDonald Herbert B. Tanowitz Murray Wittner Louis M. Weiss John P. Bilezikian Stephen A. Morris 《The Journal of eukaryotic microbiology》1998,45(1):80-86
ABSTRACT Trypomastigotes of Trypanosoma cruzi maintain an intracellular Ca2+ concentration([Ca2+]i) of 64 ± 30 nM. Equilibration of trypomastigotes in an extracellular buffer containing 0.5 mM [Ca2+]o (preloaded cells) increased [Ca2+]i < 20 nM whereas total cell Ca2+ increased by 1.5 to 2.0 pmole/cell. This amount of Ca2+ would be expected to increase [Ca2+]i to > 10 μM suggesting active sequestration of Ca2+. We tested the hypothesis that maintenance of [Ca2+]i involved both the sequestration into intracellular storage sites and extrusion into the extracellular space. Pharmacological probes known to influence [Ca2+]i through well characterized pathways in higher eukaryotic cells were employed. [Ca2+], responses in the presence or absence of [Ca2+]o were measured to asses the relative contribution of sequestration or extrusion processes in [Ca2+]i homeostasis. In the presence of 0.5 mM [Ca2+]o, the ability of several agents to increase [Ca2+]i was magnified in the order ionomycin ? nigericin > thapsigargin > monensin > valinomycin. In contrast, preloading markedly enhanced the increase in [Ca2+], observed only in response to monensin. Manoalide, an inhibitor of phospholipase A2, enhanced the accumulation of [Ca2+]i due to all agents tested, particularly ionomycin and thapsigargin. Our results suggest that sequestration of [Ca2+]i involved storage sites sensitive to monensin and ionomycin whereas extrusion of Ca2+ may involve phospholipase A2 activity. A Na+/Ca2+ exchange mechanism did not appear to contribute to Ca2+ homeostasis. 相似文献
16.
Leanna Jamieson Angel Waters Kaitlyn E. Ho Harvey Y. S. Chan Jacky T. Hung Sarah E. Webb Ching Man Chan Alan M. Shipley John G. Williamson Jon Beer Chevonne Angus Andrew L. Miller 《Journal of fish biology》2021,98(1):17-32
The elasmoid scales of anadromous sea trout Salmo trutta L. represent a significant internal reservoir of Ca2+. Although more is known about long-term remodelling of scales in response to calciotropic challenges encountered during smoltification and migration, very little is known about the contribution made by scales to the short-term, minute-to-minute regulation of Ca2+ homeostasis in the extracellular fluid (ECF) during these phases of the life cycle. This gap in the knowledge is partly due to the technical challenges involved in measuring small Ca2+ fluxes around the scales of live fish in real time. Here, this study describes exfoliating, mounting and culturing scales and their resident cells from parr, smolt and adult sea trout from a freshwater environment, as well as from adult sea trout caught in sea or brackish water. All the scales were then examined using an extracellular, non-invasive, surface-scanning Ca2+-sensitive microelectrode. The authors quantified the Ca2+ fluxes, in the absence of any systemic or local regulators, into and out of scales on both the episquamal and hyposquamal sides under different extracellular calcemic challenges set to mimic a variety of ECF-Ca2+ concentrations. Scales from the life-cycle stages as well as from adult fish taken from sea, brackish or fresh water all showed a consistent efflux or influx of Ca2+ under hypo- or hypercalcemic conditions, respectively. What were considered to be isocalcemic conditions resulted in minimal flux of Ca2+ in either direction, or in the case of adult scales, a consistent but small influx. Indeed, adult scales appeared to display the largest flux densities in either direction. These new data extend the current understanding of the role played by fish scales in the short-term, minute-to-minute homeostatic regulation of ECF-Ca2+ concentration, and are similar to those recently reported from zebrafish Danio rerio scales. This suggests that this short-term regulatory response might be a common feature of teleost scales. 相似文献
17.
Lens epithelium, when attached to its natural substratum, the lens capsule, can be maintained in culture for more than 2 weeks in a simple HEPES- and EDTA-buffered salt solution (HBS). In HBS, the epithelium shows the same characteristic phenomena of locomotion, initial retraction and respreading which in MEM plus serum precedes the inception of DNA synthesis. These phenomena have been shown to be dependent on extracellular Ca2+. 0·05 mM Ca2+ is necessary for maintaining cell-to-cell contacts of the in vivo epithelium. Higher concentrations of Ca2+ cause the epithelium to retract initially. In contrast, Mg2+ greatly favours cell-substratum interactions leading to the formation of lamellopodia and an initial spreading of the epithelium. After some hours in culture the epithelium changes markedly in response to extracellular Ca2+ and Mg2+; it respreads and flattens in the presence of Ca2+, while Mg2+ becomes less effective in maintaining cell-to-substratum contacts. Mg2+-dependent initial spreading is promoted at pH values near 7·0 but the Ca2+-dependent respreading requires an alkalinization of the salt solution. 相似文献
18.
Extracellular Calcium Sensing by Glial Cells: Low Extracellular Calcium Induces Intracellular Calcium Release and Intercellular Signaling 总被引:3,自引:0,他引:3
Abstract: Glial cells in primary mixed cultures or purified astrocyte cultures from mouse cortex respond to reduced extracellular calcium concentration ([Ca2+]e) with increases in intracellular calcium concentration ([Ca2+]i) that include single-cell Ca2+ oscillations and propagated intercellular Ca2+ waves. The rate and pattern of propagation of low [Ca2+]e-induced intercellular Ca2+ waves are altered by rapid perfusion of the extracellular medium, suggesting the involvement of an extracellular messenger in Ca2+ wave propagation. The low [Ca2+]e-induced Ca2+ response is abolished by thapsigargin and by the phospholipase antagonist U73122. The low [Ca2+]e-induced response is also blocked by replacement of extracellular Ca2+ with Ba2+, Zn2+, or Ni2+, and by 100 µM La3+. Glial cells in lowered [Ca2+]e(0.1–0.5 mM) show an increased [Ca2+]i response to bath application of ATP, whereas glial cells in increased [Ca2+]e (10–15 mM) show a decreased [Ca2+]i response to ATP. These results show that glial cells possess a mechanism for coupling between [Ca2+]e and the release of Ca2+ from intracellular stores. This mechanism may be involved in glial responses to the extracellular environment and may be important in pathological conditions associated with low extracellular Ca2+ such as seizures or ischemia. 相似文献
19.
Abhilash Krishna Liang Sun Miguel Valderrábano Philip T Palade John W ClarkJr 《Theoretical biology & medical modelling》2010,7(1):43
Background
The past thirty-five years have seen an intense search for the molecular mechanisms underlying calcium-induced calcium-release (CICR) in cardiac myocytes, with voltage clamp (VC) studies being the leading tool employed. Several VC protocols including lowering of extracellular calcium to affect Ca 2+ loading of the sarcoplasmic reticulum (SR), and administration of blockers caffeine and thapsigargin have been utilized to probe the phenomena surrounding SR Ca 2+ release. Here, we develop a deterministic mathematical model of a rat ventricular myocyte under VC conditions, to better understand mechanisms underlying the response of an isolated cell to calcium perturbation. Motivation for the study was to pinpoint key control variables influencing CICR and examine the role of CICR in the context of a physiological control system regulating cytosolic Ca 2+ concentration ([Ca 2+] myo ). 相似文献20.
Involvement of plasma membrane calcium influx in bacterial induction of the k/h and hypersensitive responses in tobacco 总被引:11,自引:7,他引:4
An early event in the hypersensitive response of tobacco to Pseudomonas syringae pv syringae is the initiation of a K+/H+ response characterized by specific plasma membrane K+ efflux, extracellular alkalinization, and intracellular acidification. We investigated the role of calcium in induction of these host responses. Suspension-cultured tobacco cells exhibited a baseline Ca2+ influx of 0.02 to 0.06 micromole per gram per hour as determined from 45Ca2+ uptake. Following bacterial inoculation, uptake rates began to increase coincidently with onset of the K+/H+ response. Rates increased steadily for 2 to 3 hours, reaching 0.5 to 1 micromole per gram per hour. This increased Ca2+ influx was prevented by EGTA and calcium channel blockers such as La3+, Co2+, and Cd2+ but not by verapamil and nifedipine. Lanthanum, cobalt, cadmium, and EGTA inhibited the K+/H+ response in both suspension-cultured cells and leaf discs and prevented hypersensitive cell death in leaf discs. We conclude that increased plasmalemma Ca2+ influx is required for the K+/H+ and hypersensitive responses in tobacco. 相似文献