Detail of "4237-93-8"

Reference

Evidence for separate peptide sequences related to the lipolytic and magnesium-accumulating activities of ACTH

Evidence for separate peptide sequences related to the lipolytic and magnesium-accumulating activities of ACTH. Analogy with adrenergic receptors. Elliott, Donald A.; Draper, Michael W.; Rizack, Martin A. (Rockefeller Univ., New York, N. Y., USA). J. Med. Chem., 20(4), 584-6 (English) 1977. CODEN: JMCMAR. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Section cross-reference(s): 34 Native adrenocorticotropin ACTH-(1-39) [9061-27-2] and ACTH-(1-24) [16960-16-0] stimulate both lipolysis and Mg accumulation in rat adipocyte plasma membrane vesicles. ACTH-(1-20) [20617-17-8] retains full lipolytic activity with minimal effect on Mg accumulation, while ACTH-(11-24) [4237-93-8] stimulates Mg accumulation but not lipolysis, indicating that the peptide sequence responsible for Mg accumulation is sep. fror the core sequence (residues 4-10).There are some commonly used reagents with their cas registry numbers 7439-95-4 and 7683-59-2 in this article. Phentolamine [50-60-2] and L-propranolol [4199-09-1] were inhibitors of Mg accumulation stimulated by ACTH-(1-39) and norepinephrine [51-41-2]. Isoproterenol [7683-59-2] stimulated Mg uptake minimally, while methoxamine-HCl [61-16-5] activity was similar to that of norepinephrine. Apparently, the mechanism by which ACTH stimultes Mg accumulation is analogous to the action of .alpha.-adrenergic agents. .

Acute in-vivo effects of adrenocorticotropin on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits: involvement of the alpha-adrenergic nervous system

Acute in-vivo effects of adrenocorticotropin on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits: involvement of the alpha-adrenergic nervous system. Knudtzon, J. (Pediatr. Res. Inst., Rikshosp., Oslo 1, Norway). J. Endocrinol., 100(3), 345-52 (English) 1984. CODEN: JOENAK. ISSN: 0022-0795. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Injection of 8.5 nmol (1-24)-ACTH [16960-16-0] i.v. increased the plasma levels of glucagon [9007-92-5], insulin [9004-10-8], glucose, and free fatty acids in rabbits. The (1-14)-ACTH-induced hyperglucagonemia and hyperinsulinemia started 3 and 20 min after the injection, resp. Similar increases in the plasma levels of glucagon, insulin, and free fatty acids were found with 5.6 nmol (1-39)-ACTH [9002-60-2] whereas (1-4)-ACTH [19405-50-6], (4-10)-ACTH [4037-01-8], (1-10)-ACTH [2791-05-1], (11-24)-ACTH [4237-93-8], (7-38)-ACTH [79748-40-6], and (18-39)-ACTH [52870-23-2] (corticotropin-like intermediate lobe peptide) injected at doses of ~8 nmol were inactive. Infusions with the a-adrenergic blocking drug, phentolamine, reduced the (1-24)-ACTH-induced hyperglucagonemia and hyperglycemia, and augmented the (1-24)-ACTH-induced hyperinsulinemia, which now became significant after 5 min. Infusions with the b-adrenergic blocking drug, propranolol, did not diminish the (1-24)-ACTH-induced effects, but killed the rabbits after 2-4 h. Thus, the acute in vivo effects of ACTH in rabbits are modulated by the involvement of a-adrenergic receptors, which increase the plasma levels of glucagon and glucose, and delay and diminish 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.