Caffeine contractures, twitch characteristics and the threshold for Ca2+-induced Ca2+ release in skeletal muscle from horses with chronic intermittent rhabdomyolysis

1993 ◽  
Vol 54 (1) ◽  
pp. 110-117 ◽  
Author(s):  
J. Beech ◽  
S. Lindborg ◽  
J.E. Fletcher ◽  
F. Lizzo ◽  
L. Tripolitis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Twitch Characteristics ◽  
Caffeine Contractures

The Effect of Lanthanum on Excitation–Contraction Coupling in Frog Skeletal Muscle

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Reduced Rate ◽  
Caffeine Contractures

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.

scholarly journals Effects of Cannabinoids on Caffeine Contractures in Slow and Fast Skeletal Muscle Fibers of the Frog

2009 ◽  
Vol 229 (2) ◽  
pp. 91-99 ◽  
Author(s):  
Miguel Huerta ◽  
Mónica Ortiz-Mesina ◽  
Xóchitl Trujillo ◽  
Enrique Sánchez-Pastor ◽  
Clemente Vásquez ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Fast Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Caffeine Contractures

BAY K 8644 and nifedipine alter halothane but not caffeine contractures of malignant hyperthermic muscle fibers

1991 ◽  
Vol 261 (4) ◽  
pp. R782-R786
Author(s):  
J. H. Williams ◽  
M. Holland ◽  
J. C. Lee ◽  
C. W. Ward ◽  
C. J. McGrath
Keyword(s):  
Skeletal Muscle ◽  
Ethylene Glycol ◽  
Onset Time ◽  
Bay K 8644 ◽  
Fiber Bundles ◽  
Tetraacetic Acid ◽  
Mechanical Responses ◽  
Resting Tension ◽  
Malignant Hyperthermia Susceptible ◽  
Caffeine Contractures

The purpose of these experiments was to determine if the Ca2+ agonist BAY K 8644 and the Ca2+ antagonist nifedipine alter the mechanical responses of malignant hyperthermia-susceptible (MHS) skeletal muscle to halothane and caffeine. Muscle fiber bundles were dissected from MHS porcine skeletal muscle and exposed to BAY K 8644 (10 microM), nifedipine (1 microM), low-Ca2+ media [Ca2+ replaced by 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid], or diltiazem (30 microM) administered alone and with halothane (3%) or caffeine (0.5-0.8 mM). When administered alone, both halothane and BAY K 8644 evoked a significant change in resting tension (i.e., contracture) of 193.7 +/- 61.0 and 51.9 +/- 21.5 mN/cm2, respectively. When administered in combination, BAY K 8644 had no effect on the magnitude of the halothane contracture (195.2 +/- 58.6 mN/cm2) but reduced its onset time from 306.7 +/- 36.3 to 105.9 +/- 8.9 s. Nifedipine, low Ca2+, and diltiazem significantly reduced the halothane contracture (103.1 +/- 30.3, 123.1 +/- 20.6, and 112.6 +/- 16.2 mN/cm2, respectively) but had no effect on its onset time. In addition, low Ca2+ reduced the magnitude of the BAY K 8644 contracture (8.2 +/- 2.1 mN/cm2). BAY K 8644 also increased contractures induced by low caffeine concentrations (0.5-2.0 mM) but did not alter contractures induced by 4.0 and 8.0 mM caffeine, whereas nifedipine, low Ca2+, and diltiazem had no effect on these contractures. These results suggest that extracellular Ca2+ influx may have some influence on halothane but not on caffeine contractures of MHS skeletal muscle.

A comparison of the effects of cationic, anionic, and neutral amphipathic agents on the contractile behaviour of frog skeletal muscle. I. Twitches and potential threshold for contraction

1984 ◽  
Vol 62 (12) ◽  
pp. 1348-1355
Author(s):  
James G. Foulks ◽  
Lillian Morishita
Keyword(s):  
Skeletal Muscle ◽  
Hydrophobic Interactions ◽  
Contractile Function ◽  
Divalent Cations ◽  
Frog Skeletal Muscle ◽  
Twitch Potentiation ◽  
Low Concentrations ◽  
Small N ◽  
Potential Threshold ◽  
Caffeine Contractures

Cationic, anionic, and neutral amphipathic agents displayed striking differences as well as similarities in their effects on the contractile function of frog skeletal muscle. Slowed repolarization during the action potential appeared to account for twitch potentiation by low concentrations of alkyl trimethylammonium and by small n-alkanols (propanol, butanol). Small n-alkanols also caused a decrease in the potential threshold for K contractures and slower relaxation of submaximum K contractures as well as enhancement of chloride withdrawal and caffeine contractures, but these effects were not observed with larger alkanols. For the ionic amphipathic agents, the direction of the changes in the relation between K0 and K-contracture tension could be accounted for on the basis of the expected changes in surface charge, but the effects of these two types of agents on the rate of relaxation of submaximum K contractures were disproportionate and with the cationic series were opposite in direction to those produced by inorganic divalent cations. The reductions in the amplitude of chloride-withdrawal contractures by cationic as well as anionic amphipaths indicated that both types of agents can impair excitation–contraction coupling. Similar depressant effects on caffeine contractures demonstrate that these responses also can be influenced by events restricted to the external lamina of the sarcolemma. It is concluded that opposite effects can be produced by similar perturbations in different regions of the sarcolemma and that electrostatic as well as hydrophobic interactions can make an important contribution to the effects of amphipathic agents on twitches and contractures in skeletal muscle.

Inositol trisphosphate enhances calcium release in skinned cardiac and skeletal muscle

1986 ◽  
Vol 250 (5) ◽  
pp. C807-C811 ◽  
Author(s):  
T. M. Nosek ◽  
M. F. Williams ◽  
S. T. Zeigler ◽  
R. E. Godt
Keyword(s):  
Skeletal Muscle ◽  
Calcium Release ◽  
Inositol Trisphosphate ◽  
Calcium Sensitivity ◽  
Fiber Bundles ◽  
Tetraacetic Acid ◽  
Contractile Apparatus ◽  
Semitendinosus Muscle ◽  
Skinned Cardiac Fibers ◽  
Caffeine Contractures

Experiments from other laboratories suggest that inositol trisphosphate (InsP3) may be involved in the excitation-contraction coupling (ECC) process of cardiac and skeletal muscle. Our results support this hypothesis. Studying fiber bundles (less than 200-microns diameter) from guinea pig papillary muscles skinned with saponin and mechanically skinned single fibers from frog semitendinosus muscle, we find that calcium-induced force oscillations (observed in solutions containing low ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid and pCa 7.0) are enhanced in magnitude and frequency by InsP3 at concentrations as low as 1 microM. InsP3 at 10 microM can often induce such oscillations in mechanically skinned frog skeletal muscle. In skinned cardiac fibers, InsP3 increases the magnitude of caffeine contractures at submaximal caffeine concentrations to a greater extent than at near-maximal caffeine concentrations. InsP3 (30 microM) has no effect on either the calcium sensitivity or maximal force generated by the contractile apparatus of skinned cardiac muscle. We conclude that InsP3 has no direct effect on the contractile machinery but that it can modulate ECC by enhancing the calcium-induced release of calcium from the sarcoplasmic reticulum, possibly from the same pool and through the same mechanism as caffeine.

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