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Related Experiment Videos

Ethanol exposure results in a transient decrease in human platelet cAMP levels: evidence for a protein kinase C

P B DePetrillo1, R M Swift

  • 1Division of Clinical Pharmacology, Brown University, Roger Williams General Hospital, Providence, Rhode Island 02908.

Alcoholism, Clinical and Experimental Research
|April 1, 1992
PubMed
Summary
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Ethanol reduces human platelet cyclic AMP (cAMP) levels, an effect mediated by increased phosphodiesterase (PDE) activity and protein kinase C (PKC) activation. This finding is crucial for understanding ethanol

Area of Science:

  • Biochemistry
  • Pharmacology
  • Hematology

Background:

  • Platelets play a crucial role in hemostasis and thrombosis.
  • Cyclic adenosine monophosphate (cAMP) is a key intracellular second messenger regulating platelet function.
  • Ethanol's effects on cellular signaling pathways, including platelet cAMP levels, are not fully elucidated.

Purpose of the Study:

  • To investigate the effect of ethanol on human platelet cyclic adenosine monophosphate (cAMP) levels.
  • To elucidate the mechanisms underlying ethanol-induced changes in platelet cAMP.
  • To determine the involvement of phosphodiesterase (PDE) and protein kinase C (PKC) in ethanol's action on platelets.

Main Methods:

  • Human platelets were incubated with varying concentrations of ethanol (2–32 mM).

Related Experiment Videos

  • Platelet cAMP levels were measured at different time points.
  • The effects of phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine (IBMX) and protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7) on ethanol's action were assessed.

    • Main Results:

    • Ethanol, at concentrations between 2 and 32 mM, significantly depressed human platelet cAMP levels in a biphasic manner, with maximal effect at 30 seconds.
    • Platelet cAMP levels returned to baseline at higher ethanol concentrations and longer incubation times.
    • The cAMP-lowering effect of ethanol was attenuated by IBMX, suggesting increased PDE activity.
    • The ethanol-induced decrease in cAMP was blocked by H7, indicating a role for PKC activation.

    Conclusions:

    • Ethanol exerts a biphasic inhibitory effect on human platelet cAMP levels.
    • The mechanism involves activation of protein kinase C (PKC) and likely an increase in phosphodiesterase (PDE) activity.
    • These findings contribute to understanding the molecular mechanisms of ethanol's impact on platelet function and hemostasis.