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Interaction between dilazep and alpha-adrenoceptors.

J Q Qian, H D Batink, P B Timmermans

    Pharmacology
    |January 1, 1984
    PubMed
    Summary
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    Dilazep, a novel antianginal drug, exhibits weak calcium antagonism and a significant bradycardic effect. Its antianginal activity may stem from this bradycardia rather than its calcium channel blocking properties.

    Area of Science:

    • Pharmacology
    • Cardiovascular Medicine
    • Medicinal Chemistry

    Background:

    • Dilazep is a novel antianginal agent with a unique chemical structure.
    • It functions as a weak calcium antagonist.

    Purpose of the Study:

    • To investigate the pharmacological effects of dilazep, focusing on its calcium antagonistic and adrenoceptor interaction properties.
    • To elucidate the mechanism underlying dilazep's antianginal activity.

    Main Methods:

    • In vivo studies in pithed rats to assess hypotensive and heart rate effects.
    • Evaluation of dilazep's antagonism against alpha 2-adrenoceptor stimulation (B-HT 920) and alpha 1-adrenoceptor stimulation (methoxamine).
    • Radioligand-binding assays to determine adrenoceptor affinity.

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    Main Results:

    • Dilazep induced transient hypotension and a pronounced, persistent reduction in heart rate in rats.
    • The drug noncompetitively antagonized alpha 2-adrenoceptor-mediated vasoconstriction but had minimal effect on alpha 1-adrenoceptor-mediated vasoconstriction.
    • Radioligand studies revealed dilazep as a very weak alpha 1-adrenoceptor antagonist with no measurable affinity for alpha 2-adrenoceptors.

    Conclusions:

    • Dilazep's calcium-antagonistic activity is weak and requires high doses.
    • The bradycardic effect of dilazep is likely a key contributor to its antianginal efficacy.
    • The antianginal mechanism of dilazep may not solely depend on its calcium antagonistic potency.