Peptide-induced emesis in dogs.
Systemic administration of apomorphine, angiotensin II, neurotensin and leucine-enkephalin induces emesis in dogs in a dose-dependent fashion. Receptors for Leu-enkephalin and angiotensin II but not apomorphine show receptor desensitization, such that a second systemic administration 5 min after the first is ineffective. Domperidone blocked the emetic response to apomorphine but not to Leu-enkephalin or angiotensin II. Naloxone selectively blocked the Leu-enkephalin response, while saralasin blocked responses to both angiotensin II and Leu-enkephalin, but not apomorphine. Chlorpromazine prevented the emetic response to all agents, suggesting a dopamine receptor in the emetic pathway on the brain side of the blood-brain barrier. In dogs with ablation of the area postrema the emetic response to apomorphine and all peptides was prevented.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001933:Brain Stem / Q000187:drug effects*; D002552:Cerebral Ventricles / Q000187:drug effects*; D004285:Dogs; D004743:Enkephalin, Leucine / Q000494:pharmacology; D009434:Neural Pathways / Q000187:drug effects; D009496:Neurotensin / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology*; D011954:Receptors, Dopamine / Q000187:drug effects; D014839:Vomiting / Q000139:chemically induced*
D010455:Peptides; D011954:Receptors, Dopamine; D000804:Angiotensin II; D009496:Neurotensin; D004743:Enkephalin, Leucine; D001058:Apomorphine