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PMID: 1963491 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Charge movement and calcium currents in skeletal muscle fibers are enhanced by GTP gamma S.

Pflugers Archiv : European journal of physiology ·Vol. 417 ·No. 1 ·1990-09-00 ·Pages 114-6

García J, Gamboa-Aldeco R, Stefani E

Abstract

G-proteins play several regulatory roles in the cell. They can modulate ionic channels directly or in association with second messengers. In skeletal muscle, G-proteins modulate the activity of calcium channels either by acting directly on the channel and/or through a cAMP-dependent phosphorylating mechanism. The activation of G-proteins by GTP gamma S can also induce force generation in skinned fibers. In this paper we studied the effect of GTP gamma S on charge movement and calcium currents (ICa) in rat and frog skeletal muscle, using the Vaseline gap technique. We observed an increase in both charge movement and ICa after the intracellular addition of 10-100 microM GTP gamma S. GDP beta S did not have any effect. Addition of protein kinase A catalytic subunit increased the ICa, probably through a phosphorylation process, but did not modify the charge movement. This suggests that protein kinase A and GTP gamma S are acting on different sites of the channel. It can be speculated that G-proteins may have a regulatory role in the excitation-contraction coupling mechanism by a direct effect on charge movement.

MeSH Terms
Animals Anura Biological Transport/physiology Calcium/metabolism,pharmacokinetics Calcium Channels/drug effects,physiology Electric Conductivity/physiology Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology Muscle Contraction/physiology Muscles/metabolism,physiology Protein Kinases/pharmacology Rats
Chemicals
Calcium Channels Guanosine 5'-O-(3-Thiotriphosphate) Protein Kinases Calcium
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
García J
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.
Gamboa-Aldeco R
Stefani E
References (19)
19 references, click to expand
  1. Restoration of excitation-contraction coupling and slow calcium current in dysgenic muscle by dihydropyridine receptor complementary DNA.
    Nature. 1988 Nov 10;336(6195):134-9 PMID: 2903448
  2. Intramembrane charge movement in frog skeletal muscle fibres. Properties of charge 2.
    J Physiol. 1987 Jun;387:489-517 PMID: 3116215
  3. Calcium channels: molecular pharmacology, structure and regulation.
    J Membr Biol. 1988 Sep;104(2):81-105 PMID: 2903935
  4. The stimulatory G protein of adenylyl cyclase, Gs, also stimulates dihydropyridine-sensitive Ca2+ channels. Evidence for direct regulation independent of phosphorylation by cAMP-dependent protein kinase or stimulation by a dihydropyridine agonist.
    J Biol Chem. 1988 Jul 15;263(20):9887-95 PMID: 2454923
  5. Phosphorylation of the 1,4-dihydropyridine receptor of the voltage-dependent Ca2+ channel by an intrinsic protein kinase in isolated triads from rabbit skeletal muscle.
    J Biol Chem. 1987 Jun 15;262(17):8333-9 PMID: 2439499
  6. Calcium currents, charge movement and dihydropyridine binding in fast- and slow-twitch muscles of rat and rabbit.
    J Physiol. 1987 Dec;393:595-617 PMID: 2451745
  7. cAMP-dependent protein kinase rapidly phosphorylates serine- 687 of the skeletal muscle receptor for calcium channel blockers.
    J Biol Chem. 1988 Oct 25;263(30):15325-9 PMID: 2844809
  8. G-protein distribution in canine cardiac sarcoplasmic reticulum and sarcolemma: comparison to rabbit skeletal muscle membranes and to brain and erythrocyte G-proteins.
    Arch Biochem Biophys. 1987 Dec;259(2):431-40 PMID: 3122662
  9. Pertussis toxin pretreatment abolishes dihydropyridine inhibition of calcium flux in the 235-1 pituitary cell line.
    Biochem Biophys Res Commun. 1988 Feb 29;151(1):361-9 PMID: 2450538
  10. Modulation of calcium channels of twitch skeletal muscle fibres of the frog by adrenaline and cyclic adenosine monophosphate.
    J Physiol. 1987 Dec;393:307-30 PMID: 2451739
  11. Molecular properties of dihydropyridine-sensitive calcium channels in skeletal muscle.
    J Biol Chem. 1988 Mar 15;263(8):3535-8 PMID: 2450086
  12. Activation of a G protein promotes agonist responses to calcium channel ligands.
    Nature. 1987 Dec 24-31;330(6150):760-2 PMID: 2447504
  13. Decay of the slow calcium current in twitch muscle fibers of the frog is influenced by intracellular EGTA.
    J Gen Physiol. 1989 Nov;94(5):953-69 PMID: 2556497
  14. beta-adrenergic receptor and adenylate cyclase in transverse tubules of skeletal muscle.
    J Biol Chem. 1978 May 10;253(9):3049-54 PMID: 205539
  15. Involvement of dihydropyridine receptors in excitation-contraction coupling in skeletal muscle.
    Nature. 1987 Feb 19-25;325(6106):717-20 PMID: 2434854
  16. Phosphorylation of the calcium antagonist receptor of the voltage-sensitive calcium channel by cAMP-dependent protein kinase.
    Proc Natl Acad Sci U S A. 1985 Apr;82(8):2528-32 PMID: 2581248
  17. Is a guanine nucleotide-binding protein involved in excitation-contraction coupling in skeletal muscle?
    EMBO J. 1986 Feb;5(2):259-62 PMID: 2940083
  18. Regulatory GTP-binding proteins: emerging concepts on their role in cell function.
    Life Sci. 1987 Jul 20;41(3):251-8 PMID: 2439867
  19. Direct coupling of a G-protein to dihydropyridine binding sites.
    Biochem Biophys Res Commun. 1988 Nov 15;156(3):1279-86 PMID: 2461198
Article Info
Journal
Pflugers Archiv : European journal of physiology
Abbr.
Pflugers Arch
ISSN
0031-6768
Published
1990-09-00
Pages
114-6
Language
English
Region
Germany
NLM ID
0154720
Subset
IM
Grants
NIAMS NIH HHS · R01-AR38970 · United States
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