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Related Experiment Videos

Phorbol esters inhibit alpha 1-adrenergic effects and decrease the affinity of liver cell alpha 1-adrenergic

S Corvera, K R Schwarz, R M Graham

    The Journal of Biological Chemistry
    |January 15, 1986
    PubMed
    Summary
    This summary is machine-generated.

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    Phorbol ester (PMA) affects calcium-dependent hormones differently. PMA blocks alpha 1-adrenergic agonist actions by reducing high-affinity binding sites in hepatocytes.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Pharmacology

    Background:

    • Calcium-dependent hormones regulate vital cellular processes.
    • Hormonal signaling pathways are complex and involve multiple receptor interactions.
    • Tumor promoters can interfere with normal cellular signaling.

    Purpose of the Study:

    • To investigate the effects of 4 beta-Phorbol 12-myristate 13-acetate (PMA) on metabolic actions induced by calcium-dependent hormones.
    • To determine how PMA influences alpha 1-adrenergic agonist, angiotensin II, and vasopressin signaling.
    • To elucidate the mechanism by which PMA inhibits hepatocyte alpha 1-adrenergic action.

    Main Methods:

    • Hormone stimulation assays measuring glycogenolysis, ureogenesis, and phosphatidylinositol labeling.

    Related Experiment Videos

  • Radioligand binding studies using [3H]prazosin and (-)-epinephrine to characterize alpha 1-adrenergic receptors.
  • Competitive inhibition studies to analyze agonist binding affinities in the presence and absence of PMA.

    • Main Results:

    • PMA blocked alpha 1-adrenergic agonist-stimulated glycogenolysis, ureogenesis, and phosphatidylinositol labeling.
    • PMA slightly increased angiotensin II-stimulated ureogenesis at low concentrations but did not affect vasopressin-induced ureogenesis.
    • PMA decreased vasopressin-stimulated phosphatidylinositol labeling but had no effect on angiotensin II-stimulated labeling.
    • PMA treatment of hepatocytes abolished the high-affinity binding sites for (-)-epinephrine, leaving only low-affinity sites.

    Conclusions:

    • PMA differentially modulates the metabolic effects of calcium-dependent hormones in hepatocytes.
    • The inhibition of alpha 1-adrenergic signaling by PMA is associated with the loss of high-affinity adrenergic receptor binding sites.
    • These findings suggest a mechanism by which tumor promoters can disrupt normal hormonal regulation.