Indication for central vagal endorphinergic control of heart rate in dogs

Microinjections of putative enkephalin releasors, veratridine (0.2 micrograms), L-Tyr-D-Arg (1 microgram) and physostigmine (1 microgram) into the nucleus ambiguus (NA) induced naloxone-reversible bradycardia in chloralosed dogs. In addition, microinjections of compounds known to inhibit enkephalin degradation: D-phenylalanine (10 micrograms), puromycin (20 ng), Gly-Gly-Phe-Met (0.5 micrograms), and captopril (20 ng) induced a naloxone-reversible bradycardia. These results are compatible with the view that an enkephalinergic mechanism is involved in the central vagal control of the heart. These experiments provide evidence that enkephalins are tonically released from nerve terminals located in the NA and that enkephalinase, amino-peptidase and possibly angiotensin I-converting enzyme, could be involved in their catabolism in vivo.