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Related Experiment Videos

Calmodulin inhibitors decrease the CRF-and AVP-induced ACTH release in vitro: interaction of calcium-calmodulin and

K Murakami, K Hashimoto, Z Ota

    Neuroendocrinology
    |July 1, 1985
    PubMed
    Summary

    N-(6-aminohexyl)-5-chloro-naphthalene-1-sulfomide (W-7) and trifluoperazine (TFP) inhibit ACTH release. These drugs impact corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) pathways differently, suggesting distinct mechanisms for ACTH stimulation.

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    Area of Science:

    • Endocrinology
    • Neuroscience
    • Cell Biology

    Background:

    • Adrenocorticotropic hormone (ACTH) release is crucial for stress response.
    • Corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) are key regulators of ACTH secretion.
    • The intracellular mechanisms underlying CRF and AVP action require further elucidation.

    Purpose of the Study:

    • To investigate the effects of W-7 and TFP on ACTH release from rat pituitary cells.
    • To differentiate the signaling pathways utilized by CRF and AVP in stimulating ACTH release.
    • To explore the roles of calcium-calmodulin and cyclic AMP in mediating these responses.

    Main Methods:

    • Primary cell cultures of rat anterior pituitary cells and pituitary halves were utilized.
    • ACTH release was measured following stimulation with synthetic ovine CRF and AVP.

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  • Intracellular cyclic AMP levels were assessed.
  • The effects of W-7 and TFP on these processes were evaluated.

    • Main Results:

    • W-7 and TFP significantly inhibited CRF- and AVP-induced ACTH release in a dose-dependent manner.
    • CRF increased cyclic AMP levels, while AVP did not.
    • W-7 inhibited CRF-induced ACTH release without affecting cyclic AMP accumulation.

    Conclusions:

    • CRF stimulates ACTH release via both calcium-calmodulin and cyclic AMP pathways.
    • AVP primarily stimulates ACTH release through the calcium-calmodulin system.
    • W-7 and TFP act as inhibitors of ACTH release, potentially by interfering with the calcium-calmodulin pathway.