Intravenous injection of 8·5 nmol (1–24)ACTH increased the plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits. The (1–24)ACTH-induced hyperglucagonaemia and hyperinsulinaemia started 3 and 20 min after the injection respectively. Similar increases in the plasma levels of glucagon, insulin and free fatty acids were found with 5·3 nmol (1–39)ACTH, whereas (1–4)ACTH, (4–10)ACTH, (1–10)ACTH, (11–24)ACTH, (7–38)ACTH and (18–39)ACTH (corticotrophin-like intermediate lobe peptide) injected at doses of approximately 8 nmol were inactive. Infusions with the alpha-adrenergic blocking drug, phentolamine, reduced the (1–24) ACTH-induced hyperglucagonaemia and hypergly-caemia, and augmented the (1–24)ACTH-induced hyperinsulinaemia, which now became significant after 5 min. Infusions with the beta-adrenergic blocking drug, propranolol, did not diminish the (1–24)ACTH-induced effects, but killed the rabbits after 2–4 h.
It is concluded that the acute in-vivo effects of ACTH in rabbits are modulated by the involvement of alpha-adrenergic receptors, which increased the plasma levels of glucagon and glucose, and delayed and diminished the ACTH-induced increases in the plasma levels of insulin. The (1–24)ACTH-induced increases in the plasma levels of free fatty acids were not influenced by the adrenergic blocking drugs.