Activation of brainstem endorphinergic neurons causes cardiovascular depression and facilitates baroreflex bradycardia

J. A. Mastrianni, M. Palkovits, G. Kunos

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Abstract

The effects of electrical stimulation of the arcuate nucleus on blood pressure, heart rate and baroreflex sensitivity were studied in urethane-anesthetized Sprague-Dawley rats. Stimulation of the mid-anterior parts of the arcuate nucleus at 80 Hz, 0.8 ms and 50-200 μA caused a biphasic, depressor/ pressor, response and moderate bradycardia. Intravenous administration of a vasopressin V1-receptor antagonist eliminated the pressor component and unmasked a pure depressor response. This depressor response could be inhibited by naltrexone, 2 mg/kg i.v., by an antiserum against β-endorphin, 100 nl injected directly into the ipsilateral nucleus tractus solitarii, or by deafferentation of the dorsal vagal complex (nucleus tractus solitarii and dorsal vagal nucleus) by an ipsilateral, dorsolateral knife-cut of the medulla oblongata. Stimulation of the arcuate nucleus at currents of 20-40 μA did not influence basal blood pressure or heart rate but potentiated the reflex bradycardia induced by phenylephrine, and this effect was completely blocked by naltrexone. It is concluded that a β-endorphin-containing pathway projecting from the arcuate nucleus to the ipsilateral dorsal vagal complex is involved in depressor cardiovascular regulation and in the facilitation of baroreflex bradycardia.

Original languageEnglish
Pages (from-to)559-566
Number of pages8
JournalNeuroscience
Volume33
Issue number3
DOIs
Publication statusPublished - 1989

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ASJC Scopus subject areas

  • Neuroscience(all)

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