Evidence for separate peptide sequences related to the lipolytic and magnesium-accumulating activities of ACTH. Analogy with adrenergic receptors

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Abstract
Native ACTH-(1-39) and ACTH-(1-24) stimulate both lipolysis and Mg accumulation in rat adipocyte plasma membrane vesicles. ACTH-(1-20) retains full lipolytic activity but has a minimal effect on Mg accumulation; ACTH-(11-24) stimulates Mg accumulation but not lipolysis. Within the ACTH molecule, the peptide sequence responsible for stimulation of Mg accumulation appears to be distinctly separate from the core sequence (residues 4-10) essential for stimulation of adenylyl cyclase activity and c[cyclic]AMP mediated lipolysis. Phentolamine, and .alpha.-adrenergic antagonist, blocks the bulk of Mg accumulation stimulated by native ACTH and norepinephrine; propranolol, a .beta.-adrenergic antagonist, blocks the earliest phase of Mg2+ uptake by these hormones but has little effect on net uptake. Isoproterenol, a .beta.-adrenergic agonist, stimulates Mg uptake minimally. The pattern of uptake stimulated by methoxamine, an .alpha.-adrenergic agonist, or ACTH-(11-24) is quite similar to that produced by native ACTH in the presence of propranolol. The receptor through which ACTH mediates stimulation of the bulk of Mg appears to be analogous to the .alpha.-adrenergic receptor through which norepinephrine stimulates this same process.

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