Dopamine D1 receptors are involved in the ACTH-induced reversal of hemorrhagic shock

AbstractIn an experimental model of volume-controlled hemorrhagic shock causing the death of all rats within 30 min, the intravenous (i.v.) bolus injection of the adrenocorticotropic hormone fragment 1-24 (ACTH-(1-24)) (160 μg/kg) induced a prompt and sustained improvement of cardiovascular and respiratory function, with 100% survival 2 h after treatment. Pretreatment with either haloperidol, 300 μg/kg i.v. (antagonist at dopamine D[1] and D[2] receptors), or (R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol hemimaleate (SCH 23390), 50 μg/kg intraperitoneally (selective antagonist at dopamine D[1] receptors), significantly inhibited the effect of ACTH-(1-24)