ACTH increases noradrenaline release in pithed rabbits with electrically stimulated sympathetic outflow.

ACTH 0.03-1 microgram/kg per min i.v. increased the noradrenaline spillover rate (the rate at which endogenous noradrenaline enters into plasma) and the plasma noradrenaline concentration in pithed rabbits with electrically stimulated sympathetic outflow. ACTH 0.1 and 1 microgram/kg per min decreased the mean arterial pressure (MAP). The effects of ACTH persisted in animals treated with propranolol. Corticosterone 10 micrograms/kg per min had no effect on the neurochemical and circulatory parameters. ACTH 0.03 and 1 microgram/kg per min increased plasma corticosterone and cortisol concentrations; the two doses of ACTH had approximately the same effect. The plasma corticosterone concentration reached after infusion of corticosterone 10 micrograms/kg per min was about twice that obtained after ACTH 0.03 or 1 microgram/kg per min. In a second series of experiments, a pressor dose of noradrenaline (1 or 2 micrograms/kg per min) was infused i.v. into pithed rabbits. ACTH 0.03 and 1 microgram/kg per min decreased blood pressure and increased heart rate in these animals. The results suggest that high doses of ACTH increase noradrenaline release by an action on postganglionic sympathetic neurons. The effect is probably not mediated through adrenal steroids. In addition, ACTH seems to decrease MAP and to increase heart rate through postsynaptic vascular and myocardial effects.