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

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 microA 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 beta-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 microA 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 beta-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.