beta 2-Adrenoceptors regulate induction of myocardial ornithine decarboxylase in mice in vivo.

Autor: Copeland JG, Larson DF, Roeske WR, Russell DH, Womble JR
Jazyk: angličtina
Zdroj: British journal of pharmacology [Br J Pharmacol] 1982 Mar; Vol. 75 (3), pp. 479-83.
DOI: 10.1111/j.1476-5381.1982.tb09164.x
Abstrakt: The pharmacological characteristics of the myocardial adrenoceptor of the mouse have been examined during embryogenesis by measuring ornithine decarboxylase (ODC, EC 4.1.1.17) induction. 2 A four fold elevation of ODC activity was observed after isoprenaline (10 mg/kg, s.c.), and enzyme activity was increased two to three fold following adrenaline (1 mg/kg, s.c.) or terbutaline given by direct injection to the foetus (10 microgram/500 mg). 3 Pretreatment with the beta-adrenoceptor antagonist, propranolol (10 mg/kg), totally blocked the increase in ODC activity. 4 Elevation of myocardial ODC activity was not inhibited by metoprolol, a relatively specific beta-adrenoceptor antagonist, at a dose of 10 mg/kg. 5 Since the increase in ODC activity was blocked by a beta-adrenoceptor antagonist (propranolol) and enzyme activity was stimulated by terbutaline, a beta 2-agonist, we conclude that beta 2-adrenoceptors are selectively coupled to the regulation of murine cardiac ODC activity following catecholamine stimulation.
Databáze: MEDLINE