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.

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.

scholarly journals Differential effects of tetracaine on charge movements and Ca2+ signals in frog skeletal muscle.

1988 ◽  
Vol 92 (5) ◽  
pp. 601-612 ◽  
Author(s):  
L Csernoch ◽  
C L Huang ◽  
G Szucs ◽  
L Kovacs
Keyword(s):  
Skeletal Muscle ◽  
Charge Transfer ◽  
Calcium Release ◽  
Charge Movement ◽  
Frog Skeletal Muscle ◽  
Semitendinosus Muscle ◽  
Contraction Coupling ◽  
Low Concentrations ◽  
Myofilament Activation ◽  
Charge Movements

The effects of tetracaine on charge movements and on antipyrylazo III signals monitoring intracellular delta [Ca2+] were compared in cut frog semitendinosus muscle fibers in a single vaseline gap-voltage clamp. Low tetracaine concentrations (25-40 microM) markedly reduced delta [Ca2+] signals and shifted the rheobase. However, they neither influenced charge movement nor that peak delta [Ca2+] value associated with the contractile threshold. Higher tetracaine concentrations (100-200 microM) partly inhibited charge movements in cut fibers. They separated a steeply voltage-sensitive charge, some of whose features resembled 'q gamma' reported in intact fibers, and whose movement preceded delta [Ca2+] signals at threshold. These findings: (a) directly confirm an earlier suggestion that tetracaine acts on steps in excitation-contraction coupling rather than myofilament activation; (b) show that tetracaine at low concentrations can directly interfere with sarcoplasmic reticular calcium release without modifying charge movement; (c) show that the tetracaine-sensitive charge, first found in intact fibers, also exists in cut fibers; and (d) make it unlikely that tetracaine-sensitive charge transfer is a consequence of Ca2+ release as suggested on earlier occasions.

scholarly journals Sphingomyelinase depresses force and calcium sensitivity of skeletal muscle contractile apparatus

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Leonardo F. Ferreira ◽  
Jennifer S. Moylan ◽  
Kenneth S. Campbell ◽  
Michael B. Reid
Keyword(s):  
Skeletal Muscle ◽  
Calcium Sensitivity ◽  
Contractile Apparatus ◽  
Muscle Contractile

Reduced Ca2+-induced Ca2+ release from skeletal muscle sarcoplasmic reticulum at low pH

1992 ◽  
Vol 70 (6) ◽  
pp. 926-930 ◽  
Author(s):  
Jay H. Williams ◽  
Christopher W. Ward
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Ions ◽  
Rate Constants ◽  
Low Ph ◽  
Fiber Bundles ◽  
Hydrogen Ions ◽  
Muscle Calcium ◽  
Caffeine Contractures

The purpose of this investigation was to determine the effects of reduced pH on Ca2+-induced Ca2+ release (CICR) from skeletal muscle sarcoplasmic reticulum (SR). Frog semitendinosus fiber bundles (1–3/bundle) were chemically skinned via saponin treatment (50 μg/mL, 20 min), which removes the sarcolemma and leaves the SR functional. The SR was first depleted of Ca2+ then loaded for 2 min at pCa (log free Ca2+ concentration) 6.6. CICR was then evoked by exposing the fibers to pCa 5–7 for 5–60 s. CICR was evoked both in the absence of ATP and Mg2+ and in the presence of β,γ-methyieneadenosine-5′-triphosphate (AMPPCP, a nonhydrolyzable form of ATP) and Mg2+. Ca2+ remaining in the SR was then assayed via caffeine (25 mM) contracture. In all cases, CICR evoked at pH 6.5 resulted in larger caffeine contractures than that evoked at 7.0, suggesting that more Ca2+ was released during CICR at the higher pH. Accordingly, rate constants for CICR were significantly greater at pH 7.0 than at pH 6.5. These results indicate that reduced pH depresses CICR from skeletal muscle SR.Key words: sarcoplasmic reticulum, skeletal muscle, calcium ions, hydrogen ions, fatigue.

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