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Related Experiment Videos

Central effect of captopril on baroreflex.

K Takeda, H Okajima, J Hayashi

    Clinical and Experimental Hypertension. Part A, Theory and Practice
    |January 1, 1987
    PubMed
    Summary

    Captopril, a converting enzyme inhibitor, causes bradycardia by enhancing central vagal activity. This effect on heart rate regulation was confirmed by blocking it with atropine and observing greater effects with central administration.

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    Area of Science:

    • Cardiovascular Pharmacology
    • Autonomic Nervous System Regulation

    Background:

    • Converting enzyme inhibitors (CEI) are used to manage hypertension.
    • Their precise effects on heart rate regulation, particularly central mechanisms, require further elucidation.

    Purpose of the Study:

    • To investigate the impact of captopril, a CEI, on heart rate regulation.
    • To determine if CEI can centrally modulate baroreflex pathways.

    Main Methods:

    • Captopril was administered intravenously and intracisternally in rats, with and without atropine pretreatment.
    • Electrical stimulation of the aortic depressor nerve (ADN) was performed in captopril-treated rats.

    Main Results:

    • Captopril induced bradycardia and lowered blood pressure, effects abolished by atropine.

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  • Intracisternal captopril caused a greater heart rate reduction than intravenous administration.
  • Captopril attenuated central vasodepressor and sympatho-inhibitory baroreflex responses but did not alter the bradycardiac component.

    • Conclusions:

    • Captopril exerts its bradycardic effects through central activation of cardiac vagal efferent activity.
    • CEI can centrally attenuate the baroreflex-mediated vasodepressor and sympatho-inhibitory responses.