beta-Endorphin central depression of respiration and circulation.

Beta-Endorphin was injected into cerebrospinal fluid of lightly anesthetized dogs. Its effects on ventilation (V), tidal volume (VT), respiratory frequency (f), preinspiratory occlusion pressure (P500), and respiratory timing of unoccluded and occluded breaths were studied during CO2 rebreathing. Blood pressure and heart rate (HR) were monitored throughout the study. beta-Endorphin produced 1) early (approximately 15 min) but temporary depression of VT-PCO2 and P500-PCO2 responses; 2) progressive hypoventilation during spontaneous breathing and progressive depression of V-PCO2 and f-PCO2 responses, which were maximal at about 75 min, followed by gradual recovery; 3) progressive hypotension and bradycardia starting at about 15 min and reaching maximal effect at about 105 min. Increased expiratory time (TE) accounted for the changes in f. TE increased in unoccluded breaths and during both preinspiratory and inflation occlusion. After vagotomy, beta-endorphin produced insignificant effect on f, TE, and HR. Naloxone itself increased P500-PCO2 response; when given during beta-endorphin effect, it reversed the hypotension, bradycardia, V-PCO2, and f-PCO2 responses and facilitated the P500-PCO2 and VT-PCO2 responses. We conclude that beta-endorphin effect is produced by both depression of specific central cardiovascular and respiratory control units and facilitation of central vagal projections.