Paralysis of frog skeletal muscle fibres by the calcium antagonist D‐600.

Eisenberg, Robert S.; McCarthy, R. T.; Milton, Richard L.

doi:10.1113/jphysiol.1983.sp014819

Cited by 98 publications

(72 citation statements)

References 35 publications

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“…Experiments in 2 H2O were made after waiting for the equilibration time (ϳ20 min) to allow a complete exchange of 2 H2O for water in the fiber. The responses in D600 were obtained in normal Ringer during the force recovery from the paralysis induced by exposing the fiber, loaded with D600, to high-potassium solution, as described previously (10,19). We also evaluated the effects of nitrate Ringer (92 mM NaCl substituted by NaNO 3) on fibers perfused with 6.25 M Dantrolene to verify the possibility of reversing the Dantrolene effect on static stiffness with a Ca 2ϩ release potentiator (21,24).…”

Section: Methodsmentioning

confidence: 99%

Non-cross-bridge calcium-dependent stiffness in frog muscle fibers

Bagni

Colombini

Geiger

et al. 2004

American Journal of Physiology-Cell Physiology

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the end of the force transient elicited by a fast stretch applied to an activated frog muscle fiber, the force settles to a steady level exceeding the isometric level preceding the stretch. We showed previously that this excess of tension, referred to as "static tension," is due to the elongation of some elastic sarcomere structure, outside the cross bridges. The stiffness of this structure, "static stiffness," increased upon stimulation following a time course well distinct from tension and roughly similar to intracellular Ca 2ϩ concentration. In the experiments reported here, we investigated the possible role of Ca 2ϩ in static stiffness by comparing static stiffness measurements in the presence of Ca 2ϩ release inhibitors (D600, Dantrolene, 2 H2O) and cross-bridge formation inhibitors [2,3-butanedione monoxime (BDM), hypertonicity]. Both series of agents inhibited tension; however, only D600, Dantrolene, and 2 H2O decreased at the same time static stiffness, whereas BDM and hypertonicity left static stiffness unaltered. These results indicate that Ca 2ϩ , in addition to promoting cross-bridge formation, increases the stiffness of an (unidentified) elastic structure of the sarcomere. This stiffness increase may help in maintaining the sarcomere length uniformity under conditions of instability.intact muscle fiber; static stiffness; tension inhibitors; titin TENSION DEVELOPMENT in intact skeletal muscle fibers after stimulation is preceded by an increase of fiber stiffness that begins during the latent period and continues throughout the whole rise in both twitch and tetanic contractions (6,8,12). Previous work (3, 5) has shown that a small portion of the muscle stiffness increase arises from a sarcomere structure(s), outside the cross bridges, whose stiffness increases upon stimulation. This non-cross-bridge stiffness contributes very little to the stiffness of the muscle fiber at moderate or high tension; however, it represents the whole muscle stiffness increase occurring during the latent period and a substantial fraction at very low tension. The presence of this stiffness was demonstrated by studying the force response to fast ramp stretches and hold, applied to a single muscle fiber at various tension levels during a twitch or a tetanus. It was found that force, after the fast transient synchronous with the stretch, settled to a steady level greater than the isometric tension preceding the stretch, until relaxation or until the fiber was returned to the original length. Because of this characteristic, the excess of tension with respect to isometric tension was referred to as static tension, whereas the ratio between static tension and stretch amplitude, measured at sarcomere level, was termed static stiffness. Experiments made on tetanic contractions in Ringer containing 1-6 mM 2,3-butanedione monoxime (BDM), an agent that strongly inhibits cross-bridge formation (4, 14) without altering static stiffness (5), showed that the structure responsible for static stiffness behaves like an Hookean elasticity loc...

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Section: Methodsmentioning

confidence: 99%

Non-cross-bridge calcium-dependent stiffness in frog muscle fibers

Bagni

Colombini

Geiger

et al. 2004

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…It has been shown previously that the presence of D600 greatly prolongs inactivation of the voltage sensors, but that it has little effect on the sensors when they are in their resting state (Eisenberg, McCarthy & Milton, 1983;Berwe, Gottschalk & Liittgau, 1987;Feldmeyer, Melzer & Pohl, 1990;Lamb & Stephenson, 1990 b). In all three 518 EFFECT OF Mg2+ ON Ca2+ RELEASE IN MUSCLE fibres examined, a single depolarization in 10 mM-Mg2+ and 20 IaM-D600 completely abolished the response to a subsequent depolarization in 1 mM-Mg2+ (e.g.…”

Section: D600 Paralysis Upon Depolarization In 10 Mm-mg2+mentioning

confidence: 99%

Effect of Mg2+ on the control of Ca2+ release in skeletal muscle fibres of the toad.

Lamb

Stephenson

1991

The Journal of Physiology

169

173

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“…The effect of dantrolene could be compensated by a higher caffeine concentration, whereas the action of ryanodine was irreversible. The Ca antagonist D-600, which is claimed to interfer with excitation-contraction coupling in skeletal muscle (Eisenberg, McCarthy & Milton, 1983), did not affect oscillations (30 ,sM-D-600). Kumbaraci & Nastuk (1982) showed that during oscillations a low-molecular-weight substance (mol.…”

Section: Pmentioning

confidence: 99%

Proceedings of the Physiological Society, 18‐19 April 1986, Sheffield Meeting: Poster Communications

1986

The Journal of Physiology

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Organ baths perfused with preheated solutions tend to have substantial temperature loss along the flow axis unless flow rates are very high and/or bath volumes very small. As both of these conditions do not suit our requirements, a bath with integrated heating facilities was designed. Adequate heat transfer and distribution were achieved by (1) employment of a round frame, (2) using stainless steel for frame and perfusion tubing, (3) inserting two sets of heating wires and the perfusion tubing in a heat-conducting solder (Ghhwiler & Bauer, 1975) and (4) connecting the tissue bath with two heat-stabilizing chambers through four (1 mm2) inlet and outlet channels. The main chamber has a diameter of 24 mm -suitable for our culture explants on round cover-slips. The bottom of the chamber consists of a round glass glued to the metal frame. Temperature is controlled by a linear thermistor. The control circuit compares the actual temperature with the preset temperature and feeds current according to that difference to the heating wires (Chabala, Sheridan, Hodge, Power & Walsh, 1985). With a flow rate of 2 ml/min it takes 7 min to achieve a preset temperature of 35 + 015 C starting from room temperature (22 'C). The uniformity of the temperature distribution in the chamber is illustrated by Fig. 1 B (flow rate, 2 ml/min; bath volume, 0 7 ml; preset temperature, 34 0 'C.

show abstract

Paralysis of frog skeletal muscle fibres by the calcium antagonist D‐600.

Cited by 98 publications

References 35 publications

Non-cross-bridge calcium-dependent stiffness in frog muscle fibers

Non-cross-bridge calcium-dependent stiffness in frog muscle fibers

Effect of Mg2+ on the control of Ca2+ release in skeletal muscle fibres of the toad.

Proceedings of the Physiological Society, 18‐19 April 1986, Sheffield Meeting: Poster Communications

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