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  • 1
    Electronic Resource
    Electronic Resource
    Identification of ATP-sensitive Potassium Channel in Frog Ventricular Myocytes (1996)
    Springer
    The journal of membrane biology 154 (1996), S. 45-51 
    Details
    ISSN: 1432-1424
    Keywords: Key words: ATP-sensitive K+ channel —Rana catesbeiana— Patch clamp — Heart ventricle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. ATP-sensitive potassium channels were found in frog ventricular myocytes using the inside-out patch-clamp technique. The channel was selectively permeable to K+. Single-channel conductance was 32.6 pS at 3.0 mm of [K+] o and 132 mm [K+] i and 77.3 pS at 114 mm [K+] o and 132 mm [K+] i . ATP did not affect single-channel conductance. The open probability of the channel was decreased by intracellular application of ATP in both the presence and absence of 2 mm MgCl2. The coexistence of Mg2+ with ATP shifts the dose-response curve for the open probability of ATP-sensitive K+ channel against ATP rightward. The shift of the curve indicates that Mg-ATP is less effective than free ATP in inhibiting the channel. An open-time histogram was fitted by a single exponential function with a time constant of 1.63 ± 0.17 msec (n= 5) in an ATP-free medium. Mean open time (1.57 ± 0.10 msec; n= 5) was not altered but the inter-burst time (closed time between bursts) lengthened in 10 μm ATP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002329900131
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  • 2
    Electronic Resource
    Electronic Resource
    Characteristics of two slow inactivation mechanisms and their influence on the sodium channel activity of frog ventricular myocytes (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 631-638 
    Details
    ISSN: 1432-2013
    Keywords: Key words Sodium channel ; Slow inactivation process ; Fast inactivation process
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Inactivation of the fast Na+ current of heart muscle occurs in two kinetically distinct phases: a fast process operating on a millisecond time scale and a considerably slower process, the kinetic properties of which have not been explored fully. In this study, we analysed the slow inactivation process in isolated frog ventricular myocytes using the whole-cell variation of the patch-clamp method. Slow inactivation of the Na+ current followed a double-exponential time course, corresponding to slow and ultraslow components of Na+ channel inactivation. The individual time constants were 2–7 s (slow component) and 40–560 s (ultraslow component). Recovery from these slow inactivation processes also followed a double-exponential time course, but was characterized by significantly briefer time constants than those for the inactivation process. The relationship between transmembrane potential and steady-state slow or ultraslow inactivation was well described by the Boltzmann equation. The membrane potential at which half the Na+ channels are inactivated (V 1/2) and the slope factor were estimated to be –48.1 and 13.6 mV, respectively, for the slow component alone. Under conditions in which the slow and ultraslow inactivation components were both present, these parameters were –53.1 and 8.7 mV respectively. When the fast and the two slow inactivation processes occurred concomitantly, the resultant steady-state inactivation curves were shifted to more negative potentials and the slope factor was decreased. Treatment with 1 mM Cd2+ externally did not affect the time course of slow inactivation, but produced a 3–7 mV depolarizing shift in its steady-state voltage dependency by virtue of cadmium’s known effect on the cell surface potential. This study has thus identified two components of slow Na+ inactivation in heart muscle, operating on a time scale of seconds (slow inactivation) and minutes (ultraslow inactivation).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050682
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  • 3
    Electronic Resource
    Electronic Resource
    Phosphorylation modulates L-type Ca channels in frog ventricular myocytes by changes in sensitivity to Mg2+ block (1998)
    Springer
    Pflügers Archiv 435 (1998), S. 329-337 
    Details
    ISSN: 1432-2013
    Keywords: Key words L-type Ca channel ; Magnesium ; Phosphorylation ; Frog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effect of phosphorylation on the intracellular Mg2+ concentration-dependent change in Ca channel activity was examined using the patch clamp technique. The kinetic changes in Ca channels induced either by phosphorylation [1 μM forskolin (FSK) plus 50 μM isobutylmethylxanthine (IBMX)] or by lowering intracellular [Mg2+] ([Mg2+]i) are qualitatively identical: an increase in both the open probability and availability of channels, as well as a decrease in the closed time without a change in the mean open time. This suggests that the mechanism for the increase in activity of Ca channels shares a common pathway of kinetic change. The concentration/response curve for the Mg2+-evoked modification of calcium channels was altered greatly by channel phosphorylation. In the external medium containing 1 μM FSK + 50 μM IBMX, Ca channels recorded with pipettes containing okadaic acid (OA) lost their sensitivity to Mg2+ in the range 1 × 10–6 M–1 × 10–3 M and remained in a fully active state. On the contrary, under basal conditions, the activity of Ca channel was strongly dependent on the internal Mg2+ over the same range of [Mg2+]. Similarly, phosphorylation of Ca channels eliminated the blocking action of guanosine triphosphate observed under basal conditions. A model is proposed in which Ca channels are equipped with regulatory gates for opening and closing the channels, and their regulation is dependent on [Mg2+]i and the degree of phosphorylation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050519
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  • 4
    Electronic Resource
    Electronic Resource
    Regulation of L- and N-types of Ca2+ channels by intracellular ATP4– in frog dorsal root ganglion neurons (1999)
    Springer
    Pflügers Archiv 438 (1999), S. 117-124 
    Details
    ISSN: 1432-2013
    Keywords: Key words ATP ; Dorsal root ganglion neurons ; L-type Ca2+ channel ; N-type Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The roles of free Mg2+ ions, ATP4– ions and Mg-ATP complexes in the regulation of N- and L-types of Ca2+ channels were studied in frog dorsal root ganglion (DRG) neurons using the whole-cell patch-clamp technique. Because Mg2+ ions interact with ATP4– ions to form Mg-ATP complexes, addition of one species can influence the concentrations of the other two. In this study their concentrations were carefully controlled by varying the concentrations of two constituents at a time while keeping the third constant. The effects of each of the three species on barium currents through L-type (I BaL) and N-type (I BaN) Ca2+ channels were plotted against its concentrations. The dose-response curves for ATP4– show that I BaL and I BaN proportionally increased with ATP4– concentrations up to 1 mM at three different Mg2+ concentrations. At a fixed concentration of ATP4–, I BaL and I BaN remained unchanged even when pMg changed from 3 to 5. Dose-response curves for I BaL and I BaN plotted against Mg-ATP concentration did not show a consistent pattern. H-7 and Mg2+ ions did not exert any blocking effect on the activity of either Ca2+ channel type, and neither dibutyryl-cAMP nor NKH-477 had any stimulating effect, suggesting that phosphorylation is not likely to be involved in ATP-induced potentiation. From these observations, it is concluded that L-type and N-type Ca2+ channels in frog DRG neurons are regulated by ATP4– ions alone, and that the neuronal Ca2+ channels are regulated by mechanisms that are different from those regulating the cardiac Ca2+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050888
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of Ca channel by intracellular Ca2+ and Mg2+ in frog ventricular cells (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 305-317 
    Details
    ISSN: 1432-2013
    Keywords: Key words L-type Ca channel ; Magnesium ; Calcium ; Ca channel potentiation ; Na ; Ca exchange
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of changing the intracellular concentrations of Ca2+ or Mg2+ ([Ca2+]i, [Mg2+]i) on Ca current (I Ca) was studied in frog ventricular myocytes using the whole-cell and cell-attached patch clamp techniques. In the physiological range of [Mg2+]i an increase in [Ca2+]i enhanced I Ca whereas at lower [Mg2+]i I Ca was suppressed. The increase in I Ca caused by Ca2+ loading was not mediated by phosphorylation since the kinase inhibitors H-8 {N-[2-(methylamino)-ethyl]-5-isoquinolinesulphonamide dihydrochloride}, staurosporine and KN-62 {1-[N,O-bis(5-isoquinolinesulphonyl)-N-methyl-1-tyrosyl]-4-phenylpiperazine} and a non-hydrolysable adenosine 5′-triphosphate analogue β,γ-methyleneadenosine 5′-triphosphate did not prevent the Ca2+-induced I Ca increase. I Ca was dramatically increased from 10 ± 6 (n = 4) to 71 ± 7 nA/nF (n = 4) when [Mg2+]i was lowered from 1.0 × 10−3 to 1.0 × 10−6 M at a [Ca2+]i of 10−8 M. The concentration response relation for inhibition of Ca channels by [Mg2+]i is modulated by [Ca2+]i. To account for the experimental results it is postulated that competitive binding of Ca2+ or Mg2+ to the Ca channel accelerates the transition of the channel from an active to a silent mode. Single-channel recordings support this hypothesis. The regulation may have clinical relevance in cytoprotection during cardiac ischaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207267
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  • 6
    Electronic Resource
    Electronic Resource
    Modulation of Ca2+ channels by intracellular Mg2+ ions and GTP in frog ventricular myocytes (1996)
    Springer
    Pflügers Archiv 432 (1996), S. 433-438 
    Details
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Under conditions of low intracellular [Mg2+] ([Mg2+]i), achieved by dialysis with pipette solutions containing ethylenediamine tetraacetic acid (EDTA), 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) and adenosine triphosphate (ATP) as chelator, calcium currents through the L-type calcium channels (I Ca) were increased in frog ventricular myocytes. Total suppression of phosphorylation by depleting the cell of ATP with a cocktail of β,γ-methyleneadenosine 5′-triphosphate (AMP-PCP) 2-deoxyglucose and carboxylcyanide-M-chlorophenylhydrazone (CCCP) did not inhibit the increase in I Ca in the Mg2+-deficient medium. Thus, the involvement of phosphorylation process in the increase in I Ca was not likely. Effective suppression of this enhancement of I Ca was achieved by the application of guanosine triphosphate (GTP). From the dose-response curve for GTP, the GTP concentration required for half-maximal inhibition (IC50) was estimated to be 4.0 μM at pMg 6. This GTP-induced suppression of I Ca is not due to the guanine nucleotide binding protein (G-protein) cascade, because both activators and inhibitors of G-protein, which are structural analogues of GTP, suppressed I Ca similarly. Treatment with pertussis toxin (PTX) did not affect the inhibitory action of Mg2+ and GTP on I Ca. GTP is therefore assumed to bind directly to the Ca2+ channel. Interaction of Mg2+ and GTP with the Ca2+ channel activated in the Mg2+-deficient medium was examined by comparing the dose/response curves for GTP at two different [Mg2+]. The IC50 for GTP suppression was estimated to be 5.7 μM at pMg 6 and 6.9 μM at pMg 5. The results suggest strongly that Mg2+ and GTP independently bind and control Ca2+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050155
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