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Related Experiment Videos

Role for PKC in the adenosine-induced decrease in shortening velocity of rat ventricular myocytes.

J W Lester1, P A Hofmann

  • 1Department of Physiology, University of Tennessee, Memphis, Tennessee 38163, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|November 22, 2000
PubMed
Summary

Adenosine receptors activate protein kinase C (PKC) signaling, which reduces heart myocyte contraction speed. Inhibiting PKC prevents this effect, confirming its role in regulating myocyte function.

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Physiology

Background:

  • Adenosine receptor activation and protein kinase C (PKC) activation both decrease rat ventricular myocyte shortening velocity (Vmax).
  • A potential link between adenosine receptors, phosphoinositide-PKC signaling, and Vmax requires further investigation.

Purpose of the Study:

  • To investigate the relationship among adenosine receptors, phosphoinositide-PKC signaling, and Vmax in rat ventricular myocytes.
  • To determine if adenosine receptor activation leads to PKC activation and subsequent Vmax reduction.

Main Methods:

  • Measurement of inositol phosphate turnover to assess signaling pathway activation.
  • Western blot analysis to detect PKC isoform translocation (cytosol to sarcolemma) as a marker of activation.

Related Experiment Videos

  • Assessment of Vmax and Ca(2+)-dependent actomyosin ATPase activity in the presence and absence of PKC inhibitors.

    • Main Results:

    • Adenosine receptor agonist R-PIA and alpha-adrenergic agonist phenylephrine increased inositol phosphate turnover.
    • R-PIA and phenylephrine induced translocation of PKC-epsilon to the sarcolemma, indicating PKC activation.
    • PKC inhibitors abolished the R-PIA-induced decrease in Vmax and actomyosin ATPase activity.

    Conclusions:

    • Adenosine receptors activate the phosphoinositide-PKC signaling pathway in rat ventricular myocytes.
    • Adenosine receptor-mediated activation of PKC is responsible for the decrease in Vmax.