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Sympathetic Potentiation of Cyclic ADP-Ribose Formation in Rat Cardiac Myocytes

  • Haruhiro Higashida
  • Jia-Sheng Zhang
  • Shigeru Yokoyama
  • Mami Noda
  • Zhen-Guo Zhong
  • Sumiko Mochida
  • Alla Egorova
Part of the Advances in Behavioral Biology book series (ABBI, volume 53)

Abstract

Sympathetic nerve excitation stimulates β-adrenergic receptors on cardiac myocytes by release of noradrenaline, leading to an increase in the contractility. This cardiostimulant effect is mediated by an increase in Ca2+ permeability resulted from cyclic AMP-dependent phosphorylation of voltage-gated ion channels (Figure 1). Opening of phosphorylated L-type Ca2+ channels and tetrodotoxin-sensitive Na+ channels results in a transient intracellular Ca2+ concentration increase ([Ca2+]i transient) which is greater than without sympathetic stimulation. The increased [Ca2+]i is further amplified by Ca2+-induced Ca2+-release (CICR) from the sarcoplasmic reticulum ryanodine receptor Ca2+ release channels, leading to strengthened contraction. In CICR in the heart, both cyclic ADP-ribose (cADP-ribose) and Ca2+ cooperatively activate type-II ryanodine receptors to release Ca2+. However, no information on the concentration of cADP-ribose after β-adrenoceptor stimulation has yet been reported (Figure 2).

Keywords

Adrenergic Receptor Ventricular Myocytes Ryanodine Receptor ADRENOCEPTOR Stimulation Adrenergic Receptor Subtype 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

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Copyright information

© Springer Science+Business Media New York 2002

Authors and Affiliations

  • Haruhiro Higashida
  • Jia-Sheng Zhang
  • Shigeru Yokoyama
  • Mami Noda
  • Zhen-Guo Zhong
  • Sumiko Mochida
  • Alla Egorova
    • 1
  1. 1.Department of Biophysical GeneticsKanazawa University Graduate School of MedicineKanazawaJapan

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