Central cardiovascular actions of D-Ala2-Met5-enkephalinamide in the rat: effects of naloxone and nucleus reticularis gigantocellularis lesion.
In pentobarbital-anesthetized rats, intraventricular administration of D-Ala2-Met5-enkephalinamide (D-Ala, 30, 100 or 300 nmol/kg) dose-dependently elicited a reduction in arterial pressure. This D-Ala-promoted hypotension was significantly antagonized by naloxone pretreatment (3 mg/kg, i.c.v.) and attenuated by bilateral focal nucleus reticularis gigantocellularis (NRGC) lesions. At higher doses, D-Ala also produced a delayed hypertension that was not only unaffected by naloxone or NRGC lesions, but was in fact potentiated by such pretreatments. We speculate that D-Ala may produce its cardiovascular effect by activating separate subclasses of opiate receptors, possibly at different neural substrates that include the NRGC.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D004347:Drug Interactions; D004744:Enkephalin, Methionine / Q000031:analogs & derivatives* / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012154:Reticular Formation / Q000502:physiology*; D013238:Stereotaxic Techniques
D009270:Naloxone; D004744:Enkephalin, Methionine; C022118:enkephalinamide-Met, Ala(2)-