title: Effects of imidazoline antagonists of alpha 2-adrenoceptors on endogenous adrenaline-induced inhibition of insulin release.
abstract: We studied the effects of adrenoceptor antagonists and imidazoline derivatives on endogenous adrenaline-induced inhibition of insulin release in anesthetized rats. The intracerebroventricular injection of neostigmine increased plasma levels of catecholamines and glucose but not insulin. Pretreatment with an i.p. injection with phentolamine caused a dose-dependent increase in insulin secretion. When atropine was coadministered with phentolamine, the phentolamine-induced increase in insulin secretion was inhibited. Neither phentolamine nor atropine affected plasma levels of catecholamine. Yohimbine and idazoxan, which are alpha 2-adrenoceptor antagonists, and tolazoline, a non-selective alpha-adrenoceptor antagonist, also reversed adrenaline-induced inhibition of insulin secretion. Phenoxybenzamine, prazosin, propranolol, and antazoline, an imidazoline without alpha 2-adrenoceptor activity, did not affect insulin levels. When agents were preinjected i.p. in rats that were given saline into the third cerebral ventricle, phentolamine and antazoline, but not yohimbine and idazoxan, increased plasma levels of insulin. The results suggest that the inhibition of insulin release induced by adrenaline was reversed by antagonism of alpha 2-adrenoceptors. Phentolamine and antazoline, both of which are imidazoline derivatives, induced insulin secretion independently of the adrenoceptors only under the resting conditions.
authors.affiliation: Third Department of Internal Medicine, Nagoya University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Hiyoshi
authors.forename: H
authors.initials: H
authors.lastname: Miura
authors.forename: K
authors.initials: K
authors.lastname: Uemura
authors.forename: H
authors.initials: H
authors.lastname: Endo
authors.forename: K
authors.initials: K
authors.lastname: Ozawa
authors.forename: N
authors.initials: N
authors.lastname: Maeda
authors.forename: T
authors.initials: T
authors.lastname: Tamagawa
authors.forename: A
authors.initials: A
authors.lastname: Iguchi
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology*; D007093:Imidazoles / Q000494:pharmacology*; D007276:Injections, Intraventricular; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010276:Parasympatholytics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D001786:Blood Glucose; D000697:Central Nervous System Stimulants; D007093:Imidazoles; D007328:Insulin; D010276:Parasympatholytics; D012965:Sodium Chloride; D001285:Atropine; D004837:Epinephrine; D010646:Phentolamine