Delta-1 opioid agonist acutely increases hypoxic tolerance

摘要: Severe, intermittent hypoxia (hypoxic conditioning) induces an acute adaptation such that survival time during a subsequent hypoxic challenge is increased. The opioid antagonist, naloxone, and the delta-selective antagonists, naltrindole 7-benzylide-nenaltrexone (BNTX), block this adaptation. current study continued pharmacological characterization of to by using selective agonists. [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (1 mg/kg s.c.), U50488H [trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeacetamide methane sulfonate]; 30 s.c.] [D-Pen2,D-Pen5]-enkephalin (DPDPE; 100 s.c.) further augmented conditioning induced increase in time. DPDPE (56.1 peptide i.v.) increased naive mice independently decreased body temperature. DPDPE-induced was blocked delta-1-selective BNTX (0.6 but not delta-2-selective (10 s.c.). However, decrease temperature either or naltrindole. These results supported our hypothesis mechanism involves endogenous delta-1 pathway demonstrated activation receptor mimicked hypoxia.