Abstract

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 hyperglycaemia, 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.

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