Beneficial effect of i.c.v. naloxone in anaphylactic shock is mediated through peripheral beta-adrenoceptive mechanisms.
Intracerebroventricular (i.c.v.) administration of 10 micrograms naloxone significantly improved survival following experimental anaphylaxis in mice. The protective effect of i.c.v. naloxone was reversed by treatments which disrupted sympathetic outflow to the adrenal medulla, i.e. ganglionic blockade by chorisondamine chloride or denervation of the adrenal glands or by inhibition of beta-adrenoceptive sites by propranolol. These results indicate that naloxone's beneficial effect in anaphylactic shock involves central actions which are peripherally mediated through activation of beta-adrenoceptive mechanisms.
D000313:Adrenal Medulla / Q000503:physiopathology*; D000707:Anaphylaxis / Q000188:drug therapy*; D000818:Animals; D002714:Chlorisondamine / Q000008:administration & dosage; D003714:Denervation; D007276:Injections, Intraventricular; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009270:Naloxone / Q000627:therapeutic use*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D009270:Naloxone; D002714:Chlorisondamine