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  • 1
    Electronic Resource
    Electronic Resource
    Simultaneous recording of Indo-1 flourescence and Na^+/Ca^2^+ exchange current reveals two components of Ca^2^+-release from sarcoplasmic reticulum of cardiac atrial myocytes.
    Amsterdam : Elsevier
    FEBS Letters 275 (1990), S. 181-184 
    Details
    ISSN: 0014-5793
    Keywords: Ca^2^+-release ; Cardiac myocyte ; Guinea-pig heart) ; Indo-1 ; Na^+/Ca^2^+-exchange ; Sarcoplasmic reticulum
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(90)81467-3
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  • 2
    Electronic Resource
    Electronic Resource
    Dual effect of the Ca^+^+ calmodulin antagonist fendiline on Ca current in single cardiac cells
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 19 (1987), S. S75 
    Details
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/S0022-2828(87)80233-X
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  • 3
    Electronic Resource
    Electronic Resource
    Nuclear calcium signalling (2000)
    Springer
    Cellular and molecular life sciences 57 (2000), S. 371-378 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. The topic of nuclear Ca2+ signalling is beset by discrepant observations of substantial nuclear/cytoplasmic gradients. The reasons why some labs have recorded such gradients, whilst other workers see equilibration of Ca2+ cyt and Ca2+ nuc using the same cells and techniques, is unexplained. Furthermore, how such gradients could arise across the NE that possesses many highly-conductive NPCs is a mystery. Although nuclei may have the capacity to be autonomous signalling entities, with functional Ca2+ release channels and an inositide cycle, the balance of evidence suggests that Ca2+ release on the inner NE does not occur during physiological stimulation. Our work suggests that elementary Ca2+ release events originating in the cytoplasm can give rise to Ca2+ nuc signals without causing elevation of the bulk cytoplasm. Clearly, the many Ca2+ signalling mechanisms that may impinge on Ca2+ nuc will remain a topic of controversy and debate for some time.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00000699
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  • 4
    Electronic Resource
    Electronic Resource
    Uber tricyclonsaure
    Amsterdam : Elsevier
    Tetrahedron Letters 3 (1962), S. 227-228 
    Details
    ISSN: 0040-4039
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0040-4039(00)70475-8
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of intracellular Ca2+ chelating compounds on inward currents caused by Ca2+ release from sarcoplasmic reticulum in guinea-pig atrial myocytes (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 296-303 
    Details
    ISSN: 1432-2013
    Keywords: Cardiac myocyte ; Ca2+ Release ; Ca2+ Current ; Na+/Ca2+ Exchange ; Ca2+ Buffering
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ca2+ release from the sarcoplasmic reticulum (SR) of mammalian cardiac myocytes occuring either due to activation by a depolarization or the resulting transmembrane Ca2+ current (I Ca), or spontaneously due to Ca2+ overload has been shown to cause inward current(s) at negative membrane potentials. In this study, the effects of different intracellular Ca2+ chelating compounds on I Ca-evoked or spontaneous Ca2+-release-dependent inward currents were examined in dialysed atrial myocytes from hearts of adult guinea-pigs by means of whole-cell voltage-clamp. As compared to dialysis with solutions containing only a low concentration of a high affinity ethylene glycol-bis(β-aminoethylether) N,N,N′,N′-tetraacetic acid (EGTA) like chelator (50–200 μM), inward membrane currents (at −50 mV) due to evoked Ca2+ release, spontaneous Ca2+ release or Ca2+ overload following long-lasting depolarizations to very positive membrane potentials are prolonged if the dialysing fluid contains a high concentration of a low affinity Ca2+ chelating compound such as citrate or free adenosine 5′-triphosphate (ATP). Without such a non-saturable Ca2+ chelator in the dialysing fluid, Ca2+-release-dependent inward currents are often oscillatory and show an irregular amplitude. With a low affinity chelator in a non-saturable concentration, discrete inward currents with constant properties can be recorded. We conclude that the variability in Ca2+-release-dependent inward current seen in single cells arises from spatial inhomogeneities of intracellular Ca2+ concentration ([Ca2+]i) due to localized saturation of endogenous and exogenous high affinity Ca2+ buffers (e.g. [2]). This can be avoided experimentally by addition of a non-saturable buffer to the intracellular solution. This condition might be useful, if properties of Ca2+ release from the SR and/ or the resulting membrane current, like for example arrhythmogenic transient inward current, are to be investigated on the single cell level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00371110
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  • 6
    Electronic Resource
    Electronic Resource
    Intracellular citrate induces regenerative calcium release from sarcoplasmic reticulum in guinea-pig atrial myocytes (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 797-804 
    Details
    ISSN: 1432-2013
    Keywords: Ca2+ release ; Sarcoplasmic reticulum Atrial myocyte ; Heart ; Citrate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ca2+ release from the sarcoplasmic reticulum was studied in voltage-clamped guinea-pig atrial myocytes. Cells were dialysed with a pipette solution containing the Ca2+ indicator 1- [2-amino-5-(6-carboxyindol-2-yl) phenoxy]-2-(2′-amino-5′-methylphenoxy) ethane-N,N,N′,N′-tetraacetic acid](Indo-1, 100 μM) and as main anion either chloride or the low-affinity Ca2+ buffer citrate. Intracellular Ca2+ transients (Cai transients) were elicited by depolarizations from a holding potential of −50 mV. In chloride-dialysed cells, Cai transients showed a bell-shaped dependence on the amplitude of the depolarizing pulse. In citratedialysed cells, membrane depolarizations were associated with a small rise in [Ca2+]i. These small changes in [Ca2+]i were either followed by a large Cai. transient or failed to induce large changes in [Ca2+]i. The peak amplitude of the large Cai transient did not vary with the amplitude of the depolarizing pulse. These results demonstrate that in the presence of intracellular chloride, Ca2+ release in atrial cells is a graded process triggered by Ca2+ influx. Using citrate as the main intracellular anoin, Ca2+ release triggered by Ca2+ entry was no longer graded but occurred in a regenerative manner. The results are discussed in terms of two models in which citrate, affects the spatial distribution of [Ca2+]i or the loading state of the sarcoplasmic reticulum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374803
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  • 7
    Electronic Resource
    Electronic Resource
    Measurement of Ca2+-release-dependent inward current reveals two distinct components of Ca2+ release from sarcoplasmic reticulum in guinea-pig atrial myocytes (1991)
    Springer
    Pflügers Archiv 417 (1991), S. 638-644 
    Details
    ISSN: 1432-2013
    Keywords: Cardiac myocyte ; Ca2+ release ; Sarcoplasmic reticulum ; Ca2+ current ; Na+/Ca2+ exchange current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ca2+ current (L-type) and inward current caused by Ca2+ release from the sarcoplasmic reticulum and carried by electrogenic Na+/Ca2+ exchange have been measured in cultured atrial myocytes from hearts of adult guinea-pigs using whole-cell voltage clamp techniques. The pipette solution, used for internal dialysis of the cells, contained a high concentration, 60 mM or 25 mM, of citrate as a non-saturable low-affinity Ca2+-chelating compound. It has been shown previously that Ca2+-release-dependent inward current under these conditions is carried by electrogenic Na+/Ca2+ exchange. Furthermore, Ca2+-release-dependent inward current (the release signal) can be completely separated from triggering Ca2+ current if brief depolarizations for activating I Ca are used. In the majority of cells that did not produce spontaneous Ca2+ release, conditions could be found that caused the release signal to be split into two components: an early component of variable amplitude and a late component of rather constant amplitude. The delay of the late component with regard to triggering I Ca was inversely related to the amplitude of the first one. Below a certain amplitude of the first component, the second one failed to be elicited. This suggests the second component to be triggered by the first one. Weakly Ca2+-buffered cells produced spontaneous Ca2+ release, resulting in irregular “transient inward currents” at constant membrane-holding potential. Synchronization by trains of step depolarizations unmasked two components also in the spontaneous release signals. In none of the cells studied was any indication of more than two components of the release signal detected. The results are discussed in terms of two distinct compartments of sarcoplasmic reticulum with different properties of Ca2+ release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00372963
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of calcium release from sarcoplasmic reticulum on membrane currents in guinea pig atrial cardioballs (1987)
    Springer
    Pflügers Archiv 410 (1987), S. 121-131 
    Details
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract (1) Ca current (I Ca) and membrane currents related to Ca-entry during activation ofI Ca have been studied in cultured atrial myocytes from hearts of adult guinea pigs by means of patch clamp pipettes. The pipettes were filled with solutions containing citrate (65 mM) as major Ca-chelating compound and Cs ions in order to block K currents. (2) In myocytes dialysed with such solutions a monophasic time course of inactivation ofI Ca is observed, which is 1–2 orders of magnitude slower as compared to studies on intact cardiac cells or cells dialysed with EGTA as only Ca-chelating compound. (3) During long-lasting or repetitive depolarization a second component ofI Ca inactivation, apart from the slow decay observed in cells dialysed with such solutions, can be seen. This component of inactivation is not related to the depolarization as such but to loading of the cells with Ca2+. Whenever the rapid component of inactivation occurs, a transient inward current (I ti) after repolarization to the holding potential (−40 to −50 mV) is recorded. Both,I Ca inactivation andI ti can be mimicked by extracellular application of caffeine (5–10 mM), suggesting both current changes to be caused by a rise in Cai due to Ca release from sarcoplasmic reticulum. In the presence of caffeine the rapid component ofI Ca-inactivation andI ti are abolished. (4) In addition toI Ca inactivation and activation ofI ti sarcoplasmic Ca release causes openings of a novel ion channel with large conductance (〉200 pS), the function of which is unknown. (5) The results are consistent with the concept of Cai-dependent inactivation of Ca current, which can be caused either by Ca-entry or by Ca-release from the SR. The transient inward current is likely to reflect a process of Ca-removal from the cell, namely Na−Ca exchange.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581904
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  • 9
    Electronic Resource
    Electronic Resource
    Bemerkungen zur Konstitution der Iso-campholsäure (1927)
    New York, NY : Wiley-Blackwell
    Helvetica Chimica Acta 10 (1927), S. 611-614 
    Details
    ISSN: 0018-019X
    Keywords: Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/hlca.19270100179
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  • 10
    Electronic Resource
    Electronic Resource
    Einleitung (1922)
    New York, NY : Wiley-Blackwell
    Journal für Praktische Chemie/Chemiker-Zeitung 105 (1922), S. 1-6 
    Details
    ISSN: 0021-8383
    Keywords: Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/prac.19221050101
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