[3H]Nitrendipine receptors as markers of a class of putative voltage-sensitive Ca2+ channels in normal human skeletal muscle and in muscle from duchenne muscular dystrophy patients

Authors

  • Dr. Claude Desnuelle MD,

    Corresponding author
    1. Clinique Rhumatologique et des Maladies Neuromusculaires, C. H. U La Timone, Marseille, France
    • Clinique Rhumatologique et des Maladies Neuromusculaires, CHU La Timone, 13385 Marseille, Cedex 5, France
    Search for more papers by this author
  • Dr. Jean-François Renaud PhD,

    1. Clinique Rhumatologique et des Maladies Neuromusculaires, and the Centre de Biochimie du C.N.R.S., Faculté des Sciences, Nice, France
    Search for more papers by this author
  • Dr. Eric Delpont MD,

    1. Clinique Rhumatologique et des Maladies Neuromusculaires, and the Centre de Biochimie du C.N.R.S., Faculté des Sciences, Nice, France
    Search for more papers by this author
  • Dr. Georges Serratrice MD,

    1. Clinique Rhumatologique et des Maladies Neuromusculaires, C. H. U La Timone, Marseille, France
    Search for more papers by this author
  • Renaud Delpont Lazdunski,

    1. Clinique Rhumatologique et des Maladies Neuromusculaires, C. H. U La Timone, Marseille, France
    Search for more papers by this author
  • Dr. Michel Lazdunski PhD

    1. Clinique Rhumatologique et des Maladies Neuromusculaires, and the Centre de Biochimie du C.N.R.S., Faculté des Sciences, Nice, France
    Search for more papers by this author

Abstract

Properties of nitrendipine receptors have been analyzed in skeletal muscle from normal young boys and boys with Duchenne muscular dystrophy (DMD). The dissociation constant (Kd) of the complex formed by nitrendipine with its specific receptors was 0.5 ± 0.1 nM in dystrophic muscle and 0.4 ± 0.1 nM in normal muscle. Maximum binding capacities Bmax were 403 ± 80 and 460 ± 60 fmol/mg protein in DMD and normal muscle, respectively. These results suggest that nitrendipine binding sites on nitrendipine-sensitive Ca2+ channel binding sites are not altered in Duchenne muscular dystrophy.

Ancillary