Ca2+ Antagonists as Tools in the Analysis of Excitation-Contraction Coupling in Skeletal Muscle Fibres

Lüttgau, Hans-Christoph; Bohle, T.; Schnier, A.

doi:10.1007/978-1-4615-3362-7_11

Cited by 7 publications

(3 citation statements)

References 26 publications

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“…However, this effect is most certainly related to secondary reactions. It is known that longer-lasting depolarizations, for example, transform the inactivated voltage sensor and probably also the Ca2+ channel into a secondary inactivated state, from which it recovers only slowly after hyperpolarization (LUttgau, Gottschalk & Berwe, 1986). These slow alterations were accelerated in Ca2+-free solutions containing Mg2' and may also be promoted by Ca2+…”

Section: Voltage Dependence Of Inactivationmentioning

confidence: 99%

The effects of dihydropyridine derivatives on force and Ca2+ current in frog skeletal muscle fibres.

Neuhaus

Rosenthal

Lüttgau

1990

The Journal of Physiology

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SUMMARY1. The effects of dihydropyridine (DHP) derivatives on current through the slow Ca2+ channel and on isometric force were investigated in short toe muscle fibres of the frog (Rana temporaria). The experiments were performed under voltage-clamp conditions with two flexible internal microelectrodes.2. The non-chiral DHP derivative nifedipine was used mainly because it allowed control measurements after the inactivation of the drug with UV light.3. In a TEA sulphate solution containing 4 mM-free Ca2+, nifedipine (1 /l4M) caused no relevant alterations in the time course of successive contractures induced by depolarizing steps to 0 mV of 3-5 min duration followed by a restoration time at -90 mV of 1-5 min.4. When external Ca2+ was replaced by Mg2+, nifedipine caused a dose-dependent shortening of contractures. The effect reached saturation at about 50 % of shortening with 1-5 ,uM-nifedipine. In the absence of divalent cations and with Na+ being the only metallic cation in the solution, shortening became more pronounced and maximum force decreased.5. The application of 2 /sm-nifedipine to a Ca2+-free, Mg2+-containing solution shifted the voltage dependence of force inactivation by 5-10 mV to more negative potentials. 6. Force activation was facilitated by nifedipine. In the presence of 2 /iMnifedipine in a Ca2+-containing solution, threshold potentials (rheobase) as negative as -75 mV were measured under microscopical observation. UV irradiation shifted the threshold potential back to the normal value of about -50 mV.7. The slow Ca2+ inward current was blocked almost completely by 5/#M-nifedipine, even when induced from negative holding potentials (-90 to -

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Section: Voltage Dependence Of Inactivationmentioning

confidence: 99%

The effects of dihydropyridine derivatives on force and Ca2+ current in frog skeletal muscle fibres.

Neuhaus

Rosenthal

Lüttgau

1990

The Journal of Physiology

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“…Whereas the effects of 1,4‐dihydropyridines on the voltage‐sensitive L‐type Ca 2+ channels are well documented, their effects on E‐C coupling in skeletal muscle are not fully understood, with reports that DHPs can have both stimulatory (Kitamura et al 1994) and inhibitory effects on E‐C coupling (Lamb & Walsh, 1987; Ríos & Brum, 1987; Neuhaus et al 1990; Hadley & Lederer, 1992; Lüttgau et al 1992; Schnier et al 1993; Posterino & Lamb, 1998).…”

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confidence: 99%

Dihydropyridine‐induced Ca²⁺ release from ryanodine‐sensitive Ca²⁺ pools in human skeletal muscle cells

Weigl

Hohenegger

Kress

2000

The Journal of Physiology

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1. Dihydropyridines (DHPs) are widely used antihypertensive drugs and inhibit excitation-contraction (E-C) coupling in vascular smooth muscle and in myocardial cells by antagonizing L-type Ca¥ channels (DHP receptors). However, contradictory reports exist about the interaction of the DHP with the skeletal muscle isoform of the DHP receptor and E-C coupling in skeletal muscle cells. [Ca¥]é. This effect could not be enhanced by further addition of nifedipine, suggesting that both DHPs act via a common signalling pathway. 5. Based on the specific mechanism of the skeletal muscle E-C coupling, we propose the stabilization of a conformational state of the DHP receptor by DHPs, which is sufficient to activate the ryanodine receptor.

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“…Neuronal (Hell et al 1993;Kostyuk & Verkhratsky, 1994) and cardiac (Fabiato, 1983) sub-types allow calcium entry during depolarization which triggers calcium release from internal stores by a 'calcium-induced calcium release' mechanism. The skeletal muscle sub-type, however, acts principally as a voltage sensor, releasing calcium directly from internal stores via a 'voltage-sensitive calcium release' mechanism so that calcium entry is not required for E-C coupling (Armstrong, 1972;Schneider & Chandler, 1973;Tanabe et al 1987;Luttgau et al 1992). Invertebrate striated muscle L-type calcium channels have been shown to function in a similar way to vertebrate cardiac muscle types, allowing calcium entry to occur for muscle contraction (calciuminduced calcium release) (Scheuer & Gilly, 1986;Inoue et al 1996;Kits & Mandelsvelder, 1996).…”

mentioning

confidence: 99%

Differential sensitivity to calciseptine of L‐type Ca²⁺ currents in a ‘lower’vertebrate (Scyliorhinus canicula), a protochordate (Branchiostoma lanceolatum) and an invertebrate (Alloteuthis subulata)

Rogers¹,

Brown²

2001

Experimental Physiology

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Ca2+ Antagonists as Tools in the Analysis of Excitation-Contraction Coupling in Skeletal Muscle Fibres

Cited by 7 publications

References 26 publications

The effects of dihydropyridine derivatives on force and Ca2+ current in frog skeletal muscle fibres.

The effects of dihydropyridine derivatives on force and Ca2+ current in frog skeletal muscle fibres.

Dihydropyridine‐induced Ca²⁺ release from ryanodine‐sensitive Ca²⁺ pools in human skeletal muscle cells

Differential sensitivity to calciseptine of L‐type Ca²⁺ currents in a ‘lower’vertebrate (Scyliorhinus canicula), a protochordate (Branchiostoma lanceolatum) and an invertebrate (Alloteuthis subulata)

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Ca2+ Antagonists as Tools in the Analysis of Excitation-Contraction Coupling in Skeletal Muscle Fibres

Cited by 7 publications

References 26 publications

The effects of dihydropyridine derivatives on force and Ca2+ current in frog skeletal muscle fibres.

The effects of dihydropyridine derivatives on force and Ca2+ current in frog skeletal muscle fibres.

Dihydropyridine‐induced Ca2+ release from ryanodine‐sensitive Ca2+ pools in human skeletal muscle cells

Differential sensitivity to calciseptine of L‐type Ca2+ currents in a ‘lower’vertebrate (Scyliorhinus canicula), a protochordate (Branchiostoma lanceolatum) and an invertebrate (Alloteuthis subulata)

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Dihydropyridine‐induced Ca²⁺ release from ryanodine‐sensitive Ca²⁺ pools in human skeletal muscle cells

Differential sensitivity to calciseptine of L‐type Ca²⁺ currents in a ‘lower’vertebrate (Scyliorhinus canicula), a protochordate (Branchiostoma lanceolatum) and an invertebrate (Alloteuthis subulata)