THE ACTIVITY METABOLISM OF MAMMALIAN SKELETAL MUSCLE IN SITU

1932 ◽  
Vol 102 (2) ◽  
pp. 481-504 ◽  
Author(s):  
E. G. Martin ◽  
J. Field ◽  
V. E. Hall
Keyword(s):  
Skeletal Muscle ◽  
Mammalian Skeletal Muscle

An integrative, in situ approach to examining K+ flux in resting skeletal muscle

2001 ◽  
Vol 79 (12) ◽  
pp. 996-1006 ◽  
Author(s):  
Michael I Lindinger ◽  
Thomas J Hawke ◽  
Lisa Vickery ◽  
Laurie Bradford ◽  
Shonda L Lipskie
Keyword(s):  
Skeletal Muscle ◽  
Drug Effects ◽  
Potassium Transport ◽  
Mammalian Skeletal Muscle ◽  
Minimal Effect ◽  
Bovine Erythrocyte ◽  
Perfusion Medium ◽  
Sodium Potassium ◽  
Unidirectional Flux

The contributions of Na+/K+-ATPase, K+ channels, and the NaK2Cl cotransporter (NKCC) to total and unidirectional K+ flux were determined in mammalian skeletal muscle at rest. Rat hindlimbs were perfused in situ via the femoral artery with a bovine erythrocyte perfusion medium that contained either 86Rb or 42K, or both simultaneously, to determine differences in ability to trace unidirectional K+ flux in the absence and presence of K+-flux inhibitors. In most experiments, the unidirectional flux of K+ into skeletal muscle (JinK) measured using 86Rb was 8–10% lower than JinK measured using 42K. Ouabain (5 mM) was used to inhibit Na+/K+-ATPase activity, 0.06 mM bumetanide to inhibit NKCC activity, 1 mM tetracaine or 0.5 mM barium to block K+ channels, and 0.05 mM glybenclamide (GLY) to block ATP-sensitive K+ (KATP) channels. In controls, JinK remained unchanged at 0.31 ± 0.03 µmol·g–1·min–1 during 55 min of perfusion. The ouabain-sensitive Na+/K+-ATPase contributed to 50 ± 2% of basal JinK, K+ channels to 47 ± 2%, and the NKCC to 12 ± 1%. GLY had minimal effect on JinK, and both GLY and barium inhibited unidirectional efflux of K+ (JoutK) from the cell through K+ channels. Combined ouabain and tetracaine reduced JinK by 55 ± 2%, while the combination of ouabain, tetracaine, and bumetanide reduced JinK by 67 ± 2%, suggesting that other K+-flux pathways may be recruited because the combined drug effects on inhibiting JinK were not additive. The main conclusions are that the NKCC accounted for about 12% of JinK, and that KATP channels accounted for nearly all of the JoutK, in resting skeletal muscle in situ.Key words: sodium potassium chloride cotransporter, NKCC, Na+/K+-ATPase, potassium channels, potassium transport, in situ rat hindlimb.

Length dependence of staircase potentiation: interactions with caffeine and dantrolene sodium

2000 ◽  
Vol 78 (4) ◽  
pp. 350-357 ◽  
Author(s):  
Dilson E Rassier ◽  
Brian R MacIntosh
Keyword(s):  
Skeletal Muscle ◽  
Gastrocnemius Muscle ◽  
Repetitive Stimulation ◽  
Mammalian Skeletal Muscle ◽  
Optimal Length ◽  
Dantrolene Sodium ◽  
Length Dependence ◽  
Before And After ◽  
Isometric Twitch

In skeletal muscle, there is a length dependence of staircase potentiation for which the mechanism is unclear. In this study we tested the hypothesis that abolition of this length dependence by caffeine is effected by a mechanism independent of enhanced Ca2+ release. To test this hypothesis we have used caffeine, which abolishes length dependence of potentiation, and dantrolene sodium, which inhibits Ca2+ release. In situ isometric twitch contractions of rat gastrocnemius muscle before and after 20 s of repetitive stimulation at 5 Hz were analyzed at optimal length (Lo), Lo - 10%, and Lo + 10%. Potentiation was observed to be length dependent, with an increase in developed tension (DT) of 78 ± 12, 51 ± 5, and 34 ± 9% (mean ± SEM), at Lo - 10%, Lo, and Lo + 10%, respectively. Caffeine diminished the length dependence of activation and suppressed the length dependence of staircase potentiation, giving increases in DT of 65±13, 53 ± 11, and 45 ± 12% for Lo - 10%, Lo, and Lo + 10%, respectively. Dantrolene administered after caffeine did not reverse this effect. Dantrolene alone depressed the potentiation response, but did not affect the length dependence of staircase potentiation, with increases in DT of 58 ± 17, 26 ± 8, and 18 ± 7%, respectively. This study confirms that there is a length dependence of staircase potentiation in mammalian skeletal muscle which is suppressed by caffeine. Since dantrolene did not alter this suppression of the length dependence of potentiation by caffeine, it is apparently not directly modulated by Ca2+ availability in the myoplasm.

Length-dependent potentiation and myosin light chain phosphorylation in rat gastrocnemius muscle

1997 ◽  
Vol 273 (1) ◽  
pp. C198-C204 ◽  
Author(s):  
D. E. Rassier ◽  
L. A. Tubman ◽  
B. R. MacIntosh
Keyword(s):  
Skeletal Muscle ◽  
Gastrocnemius Muscle ◽  
Average Rate ◽  
Muscle Length ◽  
Repetitive Stimulation ◽  
Mammalian Skeletal Muscle ◽  
Optimal Length ◽  
Regulatory Light Chains ◽  
Dependent Change

Changes in muscle length affect the degree of staircase potentiation in skeletal muscle, but the mechanism by which this occurs is unknown. In this study, we tested the hypothesis that length-dependent change in staircase is modulated by phosphorylation of the myosin regulatory light chains (RLC), since this is believed to be the main mechanism of potentiation. In situ isometric contractile responses of rat gastrocnemius muscle during 10 s of repetitive stimulation at 10 Hz were analyzed at optimal length (Lo), Lo - 10%, and Lo + 10%. The degree of enhancement of developed tension during 10 s of repetitive stimulation was observed to be length dependent, with increases of 118.5 +/- 7.8, 63.1 +/- 3.9, and 45.6 +/- 4.1% (means +/- SE) at Lo - 10%, Lo, and Lo + 10%, respectively. Staircase was accompanied by increases in the average rate of force development of 105.6 +/- 7.7, 55.6 +/- 4.1, and 37.2 +/- 4.4% for Lo - 10%, Lo, and Lo + 10%, respectively. RLC phosphorylation after 10 s of 10-Hz stimulation was higher than under resting conditions but not different among Lo - 10% (40 +/- 3.5%), Lo (35 +/- 3.5%), and Lo + 10% (41 +/- 3.5%). This study shows that there is a length dependence of staircase potentiation in mammalian skeletal muscle that may not be directly modulated by RLC phosphorylation. Interaction of RLC phosphorylation with length-dependent changes in Ca2+ release and intermyofilament spacing may explain these observations.

Ouabain stimulates unidirectional and net potassium efflux in resting mammalian skeletal muscle

2001 ◽  
Vol 79 (11) ◽  
pp. 932-941 ◽  
Author(s):  
Thomas J Hawke ◽  
Sarah Lessard ◽  
Lisa Vickery ◽  
Shonda L Lipskie ◽  
Michael I Lindinger
Keyword(s):  
Skeletal Muscle ◽  
Mammalian Skeletal Muscle ◽  
Potassium Efflux ◽  
Hindlimb Muscle ◽  
Flexor Digitorum Brevis ◽  
Baseline Values ◽  
Flexor Digitorum ◽  
Subsequent Addition

The present study compared ouabain-sensitive unidirectional K+ flux into (JinK) and out of (JoutK) perfused rat hindlimb skeletal muscle in situ and mouse flexor digitorum brevis (FDB) in vitro. In situ, 5 mM ouabain inhibited 54 ± 4% of the total JinK in 28 ± 1 min, and increased the net and unidirectional efflux of K+ within 4 min. In contrast, 1.8 mM ouabain inhibited 40 ± 8% of the total JinK in 38 ± 2 min, but did not significantly affect JoutK. In vitro, 1.8 and 0.2 mM ouabain decreased JinK to a greater extent (83 ± 5%) than in situ, but did not significantly affect 42K loss rate compared with controls. The increase in unidirectional K+ efflux (JoutK) with 5 mM ouabain in situ was attributed to increased K+ efflux through cation channels, since addition of barium (1 mM) to ouabain-perfused muscles returned JoutK to baseline values within 12 min. Perfusion with 5 mM ouabain plus 2 mM tetracaine for 30 min decreased JinK 46 ± 9% (0.30 ± 0.03 to 0.16 ± 0.02 µmol·min–1·g–1), however tetracaine was unable to abolish the ouabain-induced increase in unidirectional K+ efflux. In both rat hindlimb and mouse FDB, tetracaine had no effect on JoutK. Perfusion of hindlimb muscle with 0.1 mM tetrodotoxin (TTX, a Na+ channel blocker) decreased JinK by 15 ± 1%, but had no effect on JoutK; subsequent addition of ouabain (5 mM) decreased JinK a further 32 ± 2%. The ouabain-induced increase in unidirectional K+ efflux did not occur when TTX was perfused prior to and during perfusion with 5 mM ouabain. We conclude that 5 mM ouabain increases the unidirectional efflux of K+ from skeletal muscle through a barium and TTX-sensitive pathway, suggestive of voltage sensitive Na+ channels, in addition to inhibiting Na+/K+-ATPase activity.Key words: cardiac glycoside, Na,K pump, K+ channels, Na+ channels, perfused rat hindlimb, flexor digitorum brevis, TTX, barium, tetracaine.

Insulin-induced hyperpolarization in mammalian skeletal muscle

1989 ◽  
Vol 256 (2) ◽  
pp. C368-C374 ◽  
Author(s):  
S. T. Iannaccone ◽  
K. X. Li ◽  
N. Sperelakis ◽  
D. A. Lathrop
Keyword(s):  
Skeletal Muscle ◽  
New York ◽  
Molecular Basis ◽  
Insulin Action ◽  
Normal Group ◽  
Mammalian Skeletal Muscle ◽  
Rat Skeletal Muscle ◽  
Normal Rat ◽  
Endogenous Release

Insulin-induced hyperpolarization of up to 9 mV has been described in isolated frog [J. Physiol. Lond. 252: 43-58, 1975; Am. J. Physiol. 251 (Cell Physiol. 4): C249-C254, 1979] and mammalian (Molecular Basis of Insulin Action, New York: Plenum, 1985, p. 451-463; Am. J. Physiol. 197: 524-526, 1959; Am. J. Physiol. 198: 1066-1070, 1960) skeletal muscle. We have shown that a similar hyperpolarization occurs in situ after administration of insulin in anesthetized rats. In streptozotocin (STZ)-treated rats, insulin produced approximately 66-70% of the hyperpolarization observed in normal rat skeletal muscle in situ. Administration of ouabain in situ blocked the insulin-induced hyperpolarization in the normal group of rats and significantly blunted the effect in the STZ group. These results suggest that insulin-induced hyperpolarization in skeletal muscle results from direct activation of the Na+-K+-ATPase pump. In isolated skeletal muscle from normal and STZ rats, there was no difference in the amount of the insulin-induced hyperpolarization. There was an additive, but small, hyperpolarizing effect of insulin and isoproterenol when administered in combination, suggesting that the greater magnitude of the insulin-induced hyperpolarization observed in situ in normal rats may be due to an additive effect of injected insulin and endogenous release of epinephrine. Alternatively, STZ treatment may directly alter the Na+-K+ pump so that its response to insulin is lessened.

Electron Probe Analysis of Muscle

1982 ◽  
Vol 40 ◽  
pp. 398-401
Author(s):  
A. V. Somlyo ◽  
H. Shuman ◽  
A. P. Somlyo
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Resting State ◽  
Binding Sites ◽  
Electron Probe ◽  
Frog Skeletal Muscle ◽  
Electron Probe Analysis ◽  
Probe Analysis

Electron probe analysis of frozen dried cryosections of frog skeletal muscle, rabbit vascular smooth muscle and of isolated, hyperpermeab1 e rabbit cardiac myocytes has been used to determine the composition of the cytoplasm and organelles in the resting state as well as during contraction. The concentration of elements within the organelles reflects the permeabilities of the organelle membranes to the cytoplasmic ions as well as binding sites. The measurements of [Ca] in the sarcoplasmic reticulum (SR) and mitochondria at rest and during contraction, have direct bearing on their role as release and/or storage sites for Ca in situ.

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