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Peptide-induced emesis in dogs.

D O Carpenter, D B Briggs, N Strominger

    Behavioural Brain Research
    |March 1, 1984
    PubMed
    Summary

    Systemic administration of certain drugs induces vomiting in dogs. Receptor desensitization and specific antagonists reveal distinct pathways for apomorphine, angiotensin II, and leucine-enkephalin, implicating dopamine receptors.

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    Area of Science:

    • Neuropharmacology
    • Gastroenterology
    • Veterinary Medicine

    Background:

    • The neurochemical mechanisms underlying emesis (vomiting) are complex and involve multiple signaling pathways.
    • Understanding these pathways is crucial for developing effective antiemetic therapies.

    Purpose of the Study:

    • To investigate the specific receptors and pathways involved in drug-induced emesis in dogs.
    • To differentiate the emetic mechanisms of apomorphine, angiotensin II, neurotensin, and leucine-enkephalin.

    Main Methods:

    • Systemic administration of emetic agents (apomorphine, angiotensin II, neurotensin, leucine-enkephalin) in dogs.
    • Assessment of dose-dependent emetic responses.
    • Evaluation of receptor desensitization after repeated drug administration.
    • Pharmacological blockade of emetic responses using domperidone, naloxone, saralasin, and chlorpromazine.
    • Investigation of emetic responses in dogs with area postrema ablation.

    Main Results:

    • Apomorphine, angiotensin II, neurotensin, and leucine-enkephalin induced dose-dependent emesis.
    • Receptor desensitization was observed for leucine-enkephalin and angiotensin II, but not apomorphine.
    • Domperidone blocked apomorphine-induced emesis; naloxone blocked leucine-enkephalin; saralasin blocked angiotensin II and leucine-enkephalin.
    • Chlorpromazine blocked all emetic responses, suggesting a central dopamine receptor involvement.
    • Ablation of the area postrema abolished the emetic response to all tested agents.

    Conclusions:

    • Emesis in dogs is mediated by distinct receptor systems for apomorphine, angiotensin II, and leucine-enkephalin.
    • The area postrema is essential for mediating the emetic reflex to these agents.
    • A central dopamine receptor pathway, likely in the brainstem, plays a critical role in the emetic response.

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