[D-Met2,Pro5]enkephalinamide activates cardioinhibitory efferents in anaesthetized dogs.
[D-Met2,Pro5]enkephalinamide (DMPEA) strongly activated cardioinhibitory vagal efferents and elicited bradycardia when perfused through the cerebroventricular system of anaesthetized dogs. These effects were concentration-dependent but plateaued at an intraventricular concentration of 200 micrograms/ml. At this maximally effective concentration, the vagal discharge rate was fourfold higher and the heart rate was lowered by 28% compared to the controls. These effects were reversed by naloxone (40 micrograms/ml). There was no significant change in blood pressure. Vagal discharge rate and heart rate correlated closely and inversely with each other with r values ranging between -0.75 and -0.95. Opiate receptors in brain structures bordering the cerebroventricular system are the most likely mediators of the effects of DMPEA. The opiate receptor/endorphin system may therefore play a role in the physiological control of cardiac vagal tone and thus of heart rate.
D000200:Action Potentials / Q000187:drug effects; D000758:Anesthesia; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000378:metabolism; D004285:Dogs; D004525:Efferent Pathways / Q000187:drug effects / Q000502:physiology; D004744:Enkephalin, Methionine / Q000031:analogs & derivatives* / Q000494:pharmacology; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000294:innervation; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D014630:Vagus Nerve / Q000187:drug effects* / Q000502:physiology
D002245:Carbon Dioxide; D009270:Naloxone; D004744:Enkephalin, Methionine; C021717:enkephalin, Met(2)-ProNH2(5)-