Beta-Endorphin-Induced Cardiorespiratory Depression is Inhibited by Glycyl-L-Glutamine, A Dipeptide Derived from Beta-Endorphin Processing

摘要

Glycl-L-glutamine (Gly-L-Gin), or Beta-endorphin-(3O-31) (Beta-End- (30-31)), issynthesized through the post-translational processing of Beta-End-(1-31). Evidence that gly-L-gin is a prominent end product of Beta-End-(1-31) processing in cardioregulatory regions of rat brain prompted us to investigate whether it modulates the cardiorespiratory depression induced by central Beta-End-(1-31) injection. As shown previously, Beta-End-(1-31) (0.5 nmol) lowered mean arterial pressure (MAP) and HR when administered i.c.v. to pentobarbital-anesthetized rats. Gly-L-gin (0.3, 0.6. 1.0 and 10.0 nmol) produced a dose-related inhibition of Beta-End-(1-31)-induced hypotension, but not bradycardia, when injected i.c.v. 15 min after Beta-End-(1-31). This effect was not attributable to hydrolysis, because equimolar amounts of L-glycine and L-glutamine were ineffective.