Biochemistry and Physiology of Cardiac Calcium Channels

  • F. Hofmann
  • V. Flockerzi
  • J. Oeken
  • P. Ruth
Conference paper
Part of the Colloquium der Gesellschaft für Biologische Chemie 18.–20. April 1985 in Mosbach/Baden book series (MOSBACH, volume 36)


The voltage-dependent slow calcium channel allows the passive movement of calcium across the plasma membrane of a variety of excitable cells and regulates thereby directly or indirectly the cytosolic calcium concentration of these cells (for a review see Reuter 1984). In cardiac muscle, opening of these channels depends on the depolarization of the membrane and is facilitated by phosphorylation of a membrane protein (Osterrieder et al. 1982). In vascular smooth muscle and in other tissues, a second type of calcium channel has been postulated which is regulated directly or indirectly by hormone receptors. These channels appear to differ in many respects from the voltage-operated calcium channels. Recently, a third type of calcium channel has been described which differs markedly in its electrophysiological characteristics from the other two types (Carbone and Lux 1984, Armstrong and Matteson 1985). The calcium conductance of the voltage- and receptor-operated channel is blocked by a heterogenous group of compounds, for which the term “calcium antagonists” (Fleckenstein 1977), calcium entry blockers, or calcium channel blockers has been introduced. Among these compounds are the phenylalkylamines verapamil, gallopamil, and desmethoxyvera-pamil, the dihydropyridines nitrendipine, nimodipine, and nifedipine, and the benzothiazepine diltiazem.


Calcium Channel Calcium Channel Blocker Nucleoside Transporter High Affinity Site Calcium Entry Blocker 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1985

Authors and Affiliations

  • F. Hofmann
  • V. Flockerzi
  • J. Oeken
  • P. Ruth
    • 1
  1. 1.Physiologische ChemieMedizinische Fakultät der Universität des SaarlandesHomburg/SaarGermany

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