Literature DB >> 7070707

Cellular membrane potentials and contractile threshold in mammalian skeletal muscle susceptible to malignant hyperthermia.

E M Gallant, G A Gronert, S R Taylor.   

Abstract

An increase in external K+ can generate contractile force in muscle, and K+ contractures are an established means to determine the effect of an agent on the relation between membrane potential and mechanical activity [8]. We have used K+-contractures to further test our hypothesis [5] that abnormal cell membrane potential responses are intrinsic to skeletal muscle of Poland China pigs susceptible to malignant hyperthermia (MHS), and a nervous system is not required to initiate malignant hyperthermia (MH). Recently it has been shown that K+-induced contractures in certain skeletal and cardiac muscles might not be determined only by cellular membrane potential changes predicted by the tendency for K+ to move in accord with its electrical and concentration gradients [3, 12]. We report here that normal and diseased skeletal muscles respond differently to raised external K+, which supports the idea that the onset of the MH syndrome is determined by a defect associated with a site in muscle cells superficial to the cytoplasm rather than, as has been suggested, within the cell or in the nervous system [7]. In addition, we find that porcine skeletal muscles, like certain other muscles, produce much less force in K+ than expected from our measurements of the relationship between membrane potential and external K+.

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Year:  1982        PMID: 7070707     DOI: 10.1016/0304-3940(82)90149-5

Source DB:  PubMed          Journal:  Neurosci Lett        ISSN: 0304-3940            Impact factor:   3.046


  9 in total

Review 1.  Etiopathogenetic defect of malignant hyperthermia: hypersensitive calcium-release channel of skeletal muscle sarcoplasmic reticulum.

Authors:  P J O'Brien
Journal:  Vet Res Commun       Date:  1987       Impact factor: 2.459

Review 2.  Malignant hyperthermia: molecular defects in membrane permeability.

Authors:  K S Cheah; A M Cheah
Journal:  Experientia       Date:  1985-05-15

3.  Divergent effects of the malignant hyperthermia-susceptible Arg(615)-->Cys mutation on the Ca(2+) and Mg(2+) dependence of the RyR1.

Authors:  E M Balog; B R Fruen; N H Shomer; C F Louis
Journal:  Biophys J       Date:  2001-10       Impact factor: 4.033

4.  A malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release, and retrograde signaling to the DHPR.

Authors:  Eric Estève; José M Eltit; Roger A Bannister; Kai Liu; Isaac N Pessah; Kurt G Beam; Paul D Allen; José R López
Journal:  J Gen Physiol       Date:  2010-05-17       Impact factor: 4.086

5.  Skeletal muscle excitation-contraction coupling. II. Plasmalemma voltage control of intact bundle contractile properties in normal and malignant hyperthermic muscles.

Authors:  E M Gallant; S K Donaldson
Journal:  Pflugers Arch       Date:  1989-05       Impact factor: 3.657

6.  Skeletal muscle excitation-contraction coupling. I. Transverse tubule control of peeled fiber Ca2+-induced Ca2+ release in normal and malignant hyperthermic muscles.

Authors:  S K Donaldson; E M Gallant; D A Huetteman
Journal:  Pflugers Arch       Date:  1989-05       Impact factor: 3.657

7.  Canine malignant hyperthermia susceptibility: erythrocytic defects--osmotic fragility, glucose-6-phosphate dehydrogenase deficiency and abnormal Ca2+ homeostasis.

Authors:  P J O'Brien; G W Forsyth; D W Olexson; H S Thatte; P B Addis
Journal:  Can J Comp Med       Date:  1984-10

8.  Canine malignant hyperthermia: diagnosis of susceptibility in a breeding colony.

Authors:  P J O'brien; P H Cribb; R J White; E D Olfert; J E Steiss
Journal:  Can Vet J       Date:  1983-06       Impact factor: 1.008

9.  Barium-treated mammalian skeletal muscle: similarities to hypokalaemic periodic paralysis.

Authors:  E M Gallant
Journal:  J Physiol       Date:  1983-02       Impact factor: 5.182

  9 in total

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