Anaphylaxis-induced increase in plasma cyclic AMP dependent on endogenous catecholamines in rats.
Plasma cyclic AMP levels during anaphylactic shock in rats was studied in 7 groups of animals: (1) control rats; (2) rats with adrenomedullectomy; (3) rats treated with propranolol; (4) rats with reserpinization; (5) rats with 6-hydroxydopamine-induced chemical sympathectomy; (6) rats treated with hexamethonium, and (7) rats treated with cocaine (catecholamine uptake inhibitor). All experiments were carried out in ovalbumin-sensitized rats. Plasma cyclic AMP showed a rapid increase during anaphylactic shock in control rats. Adrenomedullectomy abolished the anaphylaxis-induced increase in plasma cyclic AMP, while hexamethonium had no effect. Propranolol caused a dose-dependent abolition of the increase. The treatment of rats with reserpine, 6-hydroxydopamine or cocaine partially inhibited the increase in plasma cyclic AMP. The results show that the adrenal medulla is the major source of catecholamines during anaphylactic shock, and that catecholamines in the adrenergic neuronal terminals may be partly responsible for the anaphylaxis-induced increase in plasma cyclic AMP.
D000313:Adrenal Medulla / Q000502:physiology*; D000707:Anaphylaxis / Q000097:blood* / Q000503:physiopathology; D000818:Animals; D002395:Catecholamines / Q000502:physiology*; D003042:Cocaine / Q000494:pharmacology; D000242:Cyclic AMP / Q000037:antagonists & inhibitors / Q000097:blood*; D006584:Hexamethonium Compounds / Q000494:pharmacology; D006892:Hydroxydopamines / Q000494:pharmacology; D008297:Male; D009411:Nerve Endings / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012110:Reserpine / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology*
D002395:Catecholamines; D006584:Hexamethonium Compounds; D006892:Hydroxydopamines; D012110:Reserpine; D011433:Propranolol; D000242:Cyclic AMP; D003042:Cocaine