Vasodepressor neurons in medulla alter cardiac contractility and cardiac output

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    Abstract

    We injected neuroexcitatory and neuroinbibitory agents into the depressor region of the caudal ventrolateral medulla of anesthetized rabbits and determined the effect on arterial pressure, myocardial contractility, cardiac output, and plasma catecholamines and neuropeptide Y. Brief excitation of the sympathoinbibitory neurons with medullary injection of L-glutamate reduced arterial pressure, peripheral vascular resistance, and myocardial contractility. Cardiac output was unaffected. Prolonged inhibition of the sympathoinhibitory neurons with medullary injection of muscimol increased arterial pressure, peripheral vascular resistance, and myocardial contractility. There was a progressive fall in cardiac output. These changes were accompanied by an increase in plasma neuropeptide Y and plasma norepinephrine, but no change in plasma epinephrine. Our findings indicate that the sympathoinhibitory vasomotor neurons in the caudal ventrolateral medulla tonically suppress the activity of sympathetic preganglionic neurons controlling myocardial contractility as well as peripheral vasomotor tone. Dysfunction of these medullary neurons could underly some forms of experimental hypertension.

    Original languageEnglish
    Pages (from-to)210-215
    Number of pages6
    JournalHypertension
    Volume21
    Issue number2
    DOIs
    Publication statusPublished - 1 Feb 1993

    Keywords

    • Cardiac output
    • Medulla oblongata
    • Myocardial contraction
    • Rabbit studies

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