Effects of twitch potentiators and repetitive stimulation on arsenazo III Ca-transients in Xenopus skeletal muscle fibers.

Ochi, Kazunori

doi:10.2170/jjphysiol.34.857

Cited by 4 publications

(3 citation statements)

References 26 publications

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“…7B) showed prolonged time course and marked potentiation of twitch tension in the presence of caffeine. The prolongation of the falling phase of the light signal was qualitatively similar to that observed by Ochi (1984), but was smaller in the present study. Time to peak light and time to peak tension were also slightly delayed by caffeine.…”

Section: Elevation Of Resting Glow and Twitch Potentiation By Caffeinesupporting

confidence: 90%

Effects of caffeine on intracellular calcium concentrations in frog skeletal muscle fibres.

Konishi

Kurihara

1987

The Journal of Physiology

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1. The mechanism of twitch potentiation by caffeine was studied in single muscle fibres dissected from m. tibialis anterior of Rana temporaria. Fibres were injected with a Ca2+-sensitive photo-protein, aequorin, and the resultant light signal and tension were simultaneously recorded. 2. In twitch responses triggered every 60 s, peaks of light and tension were maintained at a constant level. Low concentrations of caffeine (0.2-0.4 mM) potentiated twitch tension accompanied by a slight increase in light signal. 3. Although peak twitch tension was dose-dependently potentiated by caffeine, light peaks were suppressed at relatively higher concentrations of caffeine (0.6-1.5 mM) with prolonged decay of the light and tension signals. 4. Light intensity in the resting muscle (resting glow) was elevated by caffeine (0.2-1.5 mM) dose-dependently without detectable tension development. This effect of caffeine was suppressed by 0.5-1.0 mM-procaine or 10 mM-adenine, inhibitors of Ca2+-induced Ca2+ release. 5. In caffeine-treated preparations, peaks of light and tension were augmented by application of procaine (0.5-1.0 mM). Adenine (10 mM) affected the light signal in essentially the same way as procaine, but the effect varied from fibre to fibre. 6. From these results, the following hypothesis is proposed: low concentrations of caffeine directly induce Ca2+ release from sarcoplasmic reticulum (s.r.) in in the resting state, and facilitates Ca2+ release from s.r. induced by the action potential during twitch. At relatively higher concentrations of caffeine (0.6-1.5 mM), rise of resting [Ca2+]i (intracellular free Ca2+ concentration) before activation might be an important factor in twitch potentiation by caffeine. If the rise of resting [Ca2+]i induced by caffeine is inhibited by procaine and the content of Ca2+ in s.r. is well maintained, caffeine could facilitate Ca2+ release by depolarization and thus potentiate twitch tension.

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Section: Elevation Of Resting Glow and Twitch Potentiation By Caffeinesupporting

confidence: 90%

Effects of caffeine on intracellular calcium concentrations in frog skeletal muscle fibres.

Konishi

Kurihara

1987

The Journal of Physiology

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“…Hypertonic solutions, at the tonicity used here (1.4 T) on frog muscle, have an effect similar to that of BDM, mainly altering cross-bridge formation without affecting Ca 2ϩ release (21). The other group of agents has a different action mechanism.…”

Section: Discussionmentioning

confidence: 88%

“…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). Experiments were made on twitch contractions because 1) the great and fast stretches necessary to measure the static stiffness easily damaged fibers developing the full tetanic tension; and 2) tension inhibitors, especially those acting by depressing Ca 2ϩ release, have a greater effect on twitch than on tetani.…”

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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Differential effects of contractile potentiators on action potential-induced Ca2+ transients of frog and mouse skeletal muscle fibres

Caputo

Bolaños

Ramos

et al. 2016

J Muscle Res Cell Motil

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Muscle fibres, isolated from frog tibialis anterior and mouse flexor digitorum brevis (FDB) were loaded with the fast dye MagFluo-4 to study the effects of potentiators caffeine, nitrate, Zn and perchlorate on Ca transients elicited by single action potentials. Overall, the potentiators doubled the transients amplitude and prolonged by about 1.5-fold their decay time. In contrast, as shown here for the first time, nitrate and Zn, but not caffeine, activated a late, secondary component of the transient rising phase of frog but not mouse, fibres. The rise time was increased from 1.9 ms in normal solution (NR) to 3.3 ms (nitrate) and 4.4 ms (Zn). In NR, a single exponential, fitted the rising phase of calcium transients of frog (τ = 0.47 ms) and mouse (τ = 0.28 ms). In nitrate and Zn only frog transients showed a secondary exponential component, τ = 0.72 ms (nitrate) and 0.94 ms, (Zn. We suggest that nitrate and Zn activate a late slower component of the ΔF/F signals of frog but not of mouse fibres, possibly promoting Ca induced Ca release at level of the RyR3, that in frog muscle fibres are localized in the para-junctional region of the triads and are absent in mouse FDB muscle fibres.

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Effects of twitch potentiators and repetitive stimulation on arsenazo III Ca-transients in Xenopus skeletal muscle fibers.

Cited by 4 publications

References 26 publications

Effects of caffeine on intracellular calcium concentrations in frog skeletal muscle fibres.

Effects of caffeine on intracellular calcium concentrations in frog skeletal muscle fibres.

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

Differential effects of contractile potentiators on action potential-induced Ca2+ transients of frog and mouse skeletal muscle fibres

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