Some Effects of Hypertonic Solutions on Contraction and Excitation-Contraction Coupling in Frog Skeletal Muscles

Gordon, Andrew; Godt, R. E.

doi:10.1085/jgp.55.2.254

Cited by 93 publications

(91 citation statements)

References 22 publications

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“…An increase in maximum tension does accompany the left shifts of the curve induced by ionic strength reduction and reduction in phosphate concentration. Similar increases in tension with reduction in ionic strength have been reported by others for skinned fibers (Ashley and Moisescu, 1977 ;Julian and Moss, 1981 ;Gordon et al, 1973 ;Thames et al, 1974) and for intact fibers (April et al, 1968 ;Edman and Hwang, 1977 ;Gordon and Godt, 1970) . We observe a large increase in tension with reduction of phosphate from 7.5 to 0 mM in 5 mM substrate but no such increase in 0.25 mM substrate.…”

Section: Discussionsupporting

confidence: 89%

Effect of cross-bridge kinetics on apparent Ca2+ sensitivity.

Brandt¹,

Cox²,

Kawai³

et al. 1982

The Journal of General Physiology

148

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Three different ways of shifting the pCa/tension curve on the pCa axis have been studied and related to changes in the rate constants of the crossbridge cycle. The curve midpoint shifts to higher pCa's wheel the substrate (Mg-ATP) is reduced from 5 to 0.25 mM, when the phosphate concentration is reduced from 7.5 mM to 0, and when the ionic strength is reduced from 0.200 to 0.120 . The Hill coefficients of the pCa/tension curve in our standard saline (5 mM substrate, 5 mM free ATP, 7.5 mM phosphate, ionic strength 0.200, 15°C) are between 5.1 and 5.6 and fall to 3.0 with the left shift of the curve brought about by reducing both substrate and phosphate. Left shifts of the curve produced by reduction in the ionic strength do not result in a lower Hill coefficient . Reducing either substrate or phosphate is associated with a reduction in the optimal frequency for oscillatory work, but reduction in ionic strength is not so associated . Maximum tension increases with the left shift of the curve brought about by reducing phosphate concentration or ionic strength, but tension decreases with the left shift of the curve accompanying substrate concentration reduction in a phosphate-free saline . We argue that one mechanism for the observed shift of the curve along the pCa axis is the relationship between the time a cross-bridge takes to complete a cycle and the time Ca 2+ stays bound to troponin C (TnC) . If the cycle rate is decreased, a smaller fraction of TnC sites must be occupied to keep a given fraction of cross-bridges active . To illustrate this concept, we present a simplified model of the cross-bridge cycle incorporating the kinetics of Ca binding to TnC.

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Section: Discussionsupporting

confidence: 89%

Effect of cross-bridge kinetics on apparent Ca2+ sensitivity.

Brandt¹,

Cox²,

Kawai³

et al. 1982

The Journal of General Physiology

148

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“…These include administrations of tetracaine, dantrolene Na, Ca 2+ deprivation, and nifedipine (Putney and Bianchi, 1974;Huang, 1981aHuang, , 1990Huang, , 1991Hui, 1983;Bruin, Fitts, Pizarro, and Rios, 1988;Rios and Brum, 1987). The physiological effects of changes in extracellular tonicity have been attributed to changes in intracellular ionic strength arising from the consequent fiber volume change (Howarth, 1958;Dydynska and Wilkie, 1963;Blinks, 1965;Caputo, 1968;Gordon and Godt, 1970). The mechanism for their influence on charge may therefore differ from those of the pharmacological agents.…”

Section: Discussionmentioning

confidence: 99%

Intramembrane charge movements in frog skeletal muscle in strongly hypertonic solutions.

Huang

1992

The Journal of General Physiology

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Intramembrane charge movements were studied in intact, voltageclamped frog (Rana temporaria) skeletal muscle fibers in external solutions made increasingly hypertonic by addition of sucrose. The marked dependence of membrane capacitance on test potential persisted with increases in extracellnlar sucrose concentration between 350 and 500 mM. Charge movements continued to show distinguishable early monotonic (qa) decays and the strongly voltage-dependent delayed (qv) charging phases reported on earlier occasions. In contrast, a further increase to 600 mM sucrose abolished the most steeply voltage-sensitive part of the membrane capacitance. It left a more gradual variation with potential that closely resembled the function that resulted when qv charge was abolished by tetracaine in the presence of 500 mM sucrose. Charging transients were now simple monotonic (qa) decays and lacked delayed (q~) transients. Furthermore, tetracaine (2 mM) altered neither the kinetic nor the steady-state features of the charge left in 600 mM sucrose. However, Ca 2÷ current activation in the same fibers persisted through such tonicity increases under identical conditions of temperature, external solution, and holding voltage. Tonicity changes thus accomplish an independent separation of qv and qa charge as defined hitherto through their tetracaine sensitivity. Their effects on q, charge correlate with earlier observations of osmotic conditions on A[Ca 2*] signals (1987. J. Physiol. (Lond.) 383:615-627.) and the parallel effects of other agents on excitation--contraction coupling and q, charge. In contrast, they suggest that Ca 2+ current activation does not require q, charge transfer whether by itself or as part of the excitation-contraction coupling process.

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“…Increasing the tonicity of the solution bathing an intact muscle fibre, by addition of impermeant solutes such as sucrose, inhibits twitch and tetanic force responses, but has little or no effect on the propagation of action potentials (Hodgkin & Horowicz, 1957;Howarth, 1958;Gordon & Godt, 1970). This inhibition of force production is preceded by a transient contracture and accompanied by increases in the resistance to stretch, basal energy expenditure and phosphocreatine consumption and a decrease in activation heat (Gordon & Godt, 1970;Yamada, 1970;Homsher, Briggs & Wise, 1974;Clausen, Dahl-Hansen & Elbrink, 1979;Rapoport, NassarGentina & Passonneau, 1982).…”

Section: Introductionmentioning

confidence: 99%

“…This inhibition of force production is preceded by a transient contracture and accompanied by increases in the resistance to stretch, basal energy expenditure and phosphocreatine consumption and a decrease in activation heat (Gordon & Godt, 1970;Yamada, 1970;Homsher, Briggs & Wise, 1974;Clausen, Dahl-Hansen & Elbrink, 1979;Rapoport, NassarGentina & Passonneau, 1982). Exposure of a muscle to hypertonic solutions for 30 min also results in translocation of Ca2" from the terminal ci8ternae of the sarcoplasmic reticulum (SR) into the longitudinal SR (Somlyo, Shuman & Somlyo, 1977).…”

Section: Introductionmentioning

confidence: 99%

Effects of osmolality and ionic strength on the mechanism of Ca2+ release in skinned skeletal muscle fibres of the toad.

Lamb

Stephenson

Stienen

1993

The Journal of Physiology

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SUMMARY1. The effects of increased osmolality and ionic strength on the mechanism of Ca2+ release were examined in mechanically skinned skeletal muscle fibres of the toad at 23°C. Ca2+ release was induced by depolarizing the transverse tubular (T-) system by ionic substitution.2. Increasing the osmolality of the 'myoplasmic' solution about four times (to 955 mosmol/kg), by addition of 700 mm sucrose to the standard potassium (K-)HDTA solution (HDTA: hexamethylenediamine-tetraacetate), only depressed the depolarization-induced response by about 46 %. Much of this decrease could be attributed to a reduction in the Ca2+-sensitivity of the contractile proteins at this high osmolality.3. Addition of > 400 mm sucrose itself often induced substantial Ca2+ release and a transient tension response. This 'spontaneous' release was (a) greatly enhanced when the sarcoplasmic reticulum (SR) had been heavily loaded with Ca2 , (b) little affected by inactivation of the voltage sensors by prolonged or permanent depolarization of the T-system and (c) blocked by Ruthenium Red (10 ,lM).4. When both the osmolality and ionic strength were increased, by increasing the K-HDTA concentration, the depolarization-induced force was greatly reduced (to 35% at 818 mosmol/kg and 5% at 1095 mosmol/kg). Most of this reduction could be directly attributed to the substantially reduced maximum force and Caa2+ sensitivity of the contractile apparatus.5. The small amount of releasable Ca2' remaining in the SR after a single depolarization in a high-HDTA solution with 1 mm EGTA (to chelate the released Ca2+), indicated that depolarization could still elicit massive Ca2`release at high ionic strength and osmolality (at 1 mm free Mg2+).6. In contrast, when the total Mg2+ and ATP concentrations were raised about threefold (free [Mg2+] increased 2-7-fold) along with the osmolality and ionic strength, the ability of depolarization to elicit Ca2+ release was greatly hindered.7. Osmotic compression of the skinned fibres to their in situ diameter by addition of 4 % polyvinylpyrrolidone (PVP-40), substantially potentiated the depolarization-* To whom correspondence should be addressed.

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Some Effects of Hypertonic Solutions on Contraction and Excitation-Contraction Coupling in Frog Skeletal Muscles

Cited by 93 publications

References 22 publications

Effect of cross-bridge kinetics on apparent Ca2+ sensitivity.

Effect of cross-bridge kinetics on apparent Ca2+ sensitivity.

Intramembrane charge movements in frog skeletal muscle in strongly hypertonic solutions.

Effects of osmolality and ionic strength on the mechanism of Ca2+ release in skinned skeletal muscle fibres of the toad.

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