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  • 11
    Electronic Resource
    Electronic Resource
    Differential sensitivity of cardiac K(ATP) + channels to guanine nucleotides — evidence for a heterogeneous channel population (1992)
    Springer
    European biophysics journal 21 (1992), S. 299-302 
    Details
    ISSN: 1432-1017
    Keywords: Cardiac K(ATP) + channels ; GTP ; GDP ; Heart muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Abstract In cell-free patches from cultured neonatal rat cardiocytes, the cytosolic presence of GTP-γ-S (100 µmol/l) or GDP-\-S (100 µmol/1) activated K(ATP) + channels. GTP-γ-S required cytosolic Mg++, suggesting that an activated G-protein causes the increase in open probability. The great variations of the channel response to GTP-γ-S and GDP-\-S indicates that cardiac K(ATP) + channels represent a heterogeneous family.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00185124
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  • 12
    Electronic Resource
    Electronic Resource
    Modulation of single cardiac Na+ channels by cytosolic Mg++ ions (1991)
    Springer
    European biophysics journal 20 (1991), S. 223-228 
    Details
    ISSN: 1432-1017
    Keywords: Na+ channel gating ; Internal bivalent cations ; Negative surface charges ; DPI-modification
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Abstract Elementary Na+ currents were recorded in inside-out patches excised from cultured neonatal rat heart myocytes in order to study the influence of cytosolic Mg++ and other bivalent cations present at the cytoplasmic membrane surface on cardiac Na+ channel gating. Exposing the cytoplasmic membrane surface to a Mg++-free environment shortened the open state of cardiac Na+ channels significantly. τopen declined to 62±2% of the value obtained at 5 mmol/l Mgi ++. Other channel properties including the tendency to reopen and the elementary current size either changed insignificantly within a 10% range or remained completely unchanged. An almost identical change of τopen can be caused by switching from a Mn++ (5 mmol/l) containing internal solution to a Mn++-free internal solution. But τopen failed to significantly respond to a variation in internal Ni++ from 5 mmol/l to 0 mmol/l. The same response to internal Mg++ withdrawal was obtained with (−)-DPI-modified, non-inactivating Na+ channels, indicating that the exit rate from the open state remains as sensitive to cytosolic Mg++ variations as in normal Na+ channels with operating inactivation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00183459
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  • 13
    Electronic Resource
    Electronic Resource
    Conformational mapping of the cytosolic linker between domains III and IV of the cardiac Na^+ channel protein and binding studies with a site-directed channel modifying antibody
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Protein Structure and Molecular 1206 (1994), S. 263-271 
    Details
    ISSN: 0167-4838
    Keywords: Cardiac Na^+ channel ; Circular dichroism ; Cytosolic linker ; Epitope mapping ; Na^+ inactivation ; Secondary structure ; Site-directed antibody
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0167-4838(94)90217-8
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  • 14
    Electronic Resource
    Electronic Resource
    Characterization of the sensitivity of cardiac outwardly-rectifying K+ channels to class III antiarrhythmics: the influence of inhibitory sulfonamide derivatives (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 313-321 
    Details
    ISSN: 1432-1912
    Keywords: Single 66 pS K+ channels ; Upregulation Channel blockade ; HE93 ; Sotalol ; Glibenclamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Elementary K+ currents through cardiac 66 pS outwardly-rectifying K+ channels isolated from cultured neonatal rat cardiocytes were recorded in the inside-out patch configuration. By analyzing the influence of inhibitory sulfonamide derivatives, the block phenomenology evoked by these class III antiarrhythmic drugs was studied. After isolation from their cellular environment, K+ (outw.-react.) channels became usually upregulated so that open probability increased with time to reach, within 3 min or longer, a several-fold enhanced steady state level. Nevertheless, the novel sulfonamide derivative HE93 (10–100 μmol/l) depressed NP o significantly within some hundred milliseconds on cytosolic administration with a calculated IC50 value of 38 μmol/1. Drug-induced channel blockade mainly emerged from an increased life time of the prolonged C2-state; τclosed (2) rose (at 100 μmol/l) to 269 ± 20%. A C1–C2 reaction scheme can adequately describe closed time kinetics in the presence of HE93 but the occurrence of a specific, drug-evolved ultralong ( $$\bar 〉$$ 60 ms) C-state and mainly underlying the NP o depression cannot be excluded. Sotalol (100 μmo1/1) caused the same block phenomenology although a 2.6-fold larger IC50 value (half maximal inhibitory concentration) suggests a smaller potency to depress channel activity. Despite a close structural relationship with the both compounds HE93 and sotalol, glibenclamide (100 μmol/l) exerted no significant inhibitory influence (IC50 = 530 μmo1/1 on K+ channel activity. Instead, this sulfonylurea interfered with open K+ channels with an association rate constant of 8.2 ± 3.8 × 106 mol−1 s−1 to shorten their 0-state, as a sign of open channel blockade. Thus, cardiac K+ outw.-rect.) channels discriminate among these drugs which provides functional evidence in support of the idea that they accomodate multiple drug receptors, one of them involved in depressing channel activity and the other receptor involved in influencing open state kinetics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168563
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  • 15
    Electronic Resource
    Electronic Resource
    Characterization of the sensitivity of cardiac outwardly-rectifying K+ channels to class III antiarrhythmics: the influence of inhibitory sulfonamide derivatives (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 313-321 
    Details
    ISSN: 1432-1912
    Keywords: Key words Single 66 pS K+ channels ; Upregulation ; Channel blockade ; HE93 ; Sotalol ; Glibenclamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Elementary K+ currents through cardiac 66 pS outwardly-rectifying K+ channels isolated from cultured neonatal rat cardiocytes were recorded in the inside-out patch configuration. By analyzing the influence of inhibitory sulfonamide derivatives, the block phenomenology evoked by these class III antiarrhythmic drugs was studied. After isolation from their cellular environment, K+  (outw.-rect.) channels became usually upregulated so that open probability increased with time to reach, within 3 min or longer, a several-fold enhanced steady state level. Nevertheless, the novel sulfonamide derivative HE93 (10–100 μmol/l) depressed NP o significantly within some hundred milliseconds on cytosolic administration with a calculated IC50 value of 38 μmol/l. Drug-induced channel blockade mainly emerged from an increased life time of the prolonged C2-state; τclosed (2) rose (at 100 μmol/l) to 269±20%. A C1–C2 reaction scheme can adequately describe closed time kinetics in the presence of HE93 but the occurrence of a specific, drug-evoked ultralong (?60 ms) C-state and mainly underlying the NP o depression cannot be excluded. Sotalol (100 μmol/l) caused the same block phenomenology although a 2.6-fold larger IC50 value (half maximal inhibitory concentration) suggests a smaller potency to depress channel activity. Despite a close structural relationship with the both compounds HE93 and sotalol, glibenclamide (100 μmol/l) exerted no significant inhibitory influence (IC50=530 μmol/l) on K+ channel activity. Instead, this sulfonylurea interfered with open K+ channels with an association rate constant of 8.2±3.8×106 mol-1 s-1 to shorten their 0-state, as a sign of open channel blockade. Thus, cardiac K+ (outw.-rect.) channels discriminate among these drugs which provides functional evidence in support of the idea that they accomodate multiple drug receptors, one of them involved in depressing channel activity and the other receptor involved in influencing open state kinetics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168563
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  • 16
    Electronic Resource
    Electronic Resource
    Responsiveness of cardiac Na+ channels to antiarrhythmic drugs: The role of inactivation (1991)
    Springer
    The journal of membrane biology 122 (1991), S. 267-278 
    Details
    ISSN: 1432-1424
    Keywords: single cardiac Na+ channels ; open-state kinetics ; drug-induced blockade ; (-)-DPI
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Elementary Na+ currents were recorded at 9°C in inside-out patches from cultured neonatal rat heart myocytes. In characterizing the sensitivity of cooled, slowly inactivating cardiac Na+ channels to several antiarrhythmic drugs including propafenone, lidocaine and quinidine, the study aimed to define the role of Na+ inactivation for open channel blockade. In concentrations (1–10 μmol/liter) effective to depressNP o significantly, propafenone completely failed to influence the open state of slowly inactivating Na+ channels. With 1 μmol/liter, τopen changed insignificantly to 96±7% of the control. Even a small number of ultralong openings of 6 msec or longer exceeding τopen of the whole ensemble several-fold and attaining τopen (at −45 mV) in cooled, (-)-DPI-modified, noninactivating Na+ channels proved to be drug resistant and could not be flicker-blocked by 10 μmol/liter propafenone. The same drug concentration induced in(-)-DPI-modified Na+ channels a discrete block with association and dissociation rate constants of 16.1 ± 5.3 × 106 mol−1 sec−1 and 675 ± 25 sec−1, respectively. Quinidine, known to have a considerable affinity for activated Na+ channels, in lower concentrations (5 μmol/liter) left τopen unchanged or reduced, in higher concentrations (10 μmol/liter) τopen only slightly to 81% of the predrug value whereasNP o declined to 30%, but repetitive blocking events during the conducting state could never be observed. Basically the same drug resistance of the open state was seen in cardiac Na+ channels whose open-state kinetics had been modulated by the cytoplasmic presence of F− ions. But in this case, propafenone reduced reopening and selectively abolished a long-lasting open state. This drug action is unlikely related to the inhibitory effect onNP o since hyperpolarization and the accompanying block attenuation did not restore the channel kinetics. It is concluded that cardiac Na+ channels cannot be flicker-blocked by antiarrhythmic drugs unless Na+ inactivation is removed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871427
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  • 17
    Electronic Resource
    Electronic Resource
    Differential response of DPI-modified cardiac Na+ channels to antiarrhythmic drugs: No flicker blockade by lidocaine (1992)
    Springer
    The journal of membrane biology 126 (1992), S. 257-263 
    Details
    ISSN: 1432-1424
    Keywords: noninactivating cardiac Na+ channels ; class 1 antiarrhythmic drugs ; INa depression ; drug-induced block
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Elementary Na+ currents were recorded in cell attached patches from short-time cultured neonatal cardiocytes in order to test the hypothesis whether the open state of DPI-modified, noninactivating cardiac Na+ channels is basically sensitive to blocking drug molecules such as antiarrhythmics. Lidocaine (300 μmol/liter) effectively reduced the open probability of cardiac Na+ channels and, at a stimulation rate of 1 Hz, depressed the reconstructed macroscopic peak I Na to 40+ 3.5% of the predrug value. The same drug concentration failed to influence DPI-modified Na+ channels. Their open state proved almost insensitive to lidocaine. τopen decreased only slightly to 85 ±2%. Still more importantly, the number of transitions between the conducting and a nonconducting configuration did not increase. At −40 mV, lidocaine may interfere with the open state with an association rate constant of 1.3×105 mol−1sec−1 which is about two orders of magnitude smaller than the rate constant obtained with propafenone or prajmalium. Moreover, propafenone (10–20 μmol/liter) or prajmalium (30 μmol/liter) led to a tremendous increase in the number of transitions between the open and a nonconducting configuration. Lidocaine also failed to evoke a fast flicker blockade with reaction kinetics in the microsecond range. It is concluded that DPI-modified cardiac Na+ channels discriminate between lidocaine and other antiarrhythmic drugs. As a tentative explanation, this might be indicative for multiple binding sites for those drugs in cardiac Na+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00232322
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