β 2‐ADRENOCEPTORS REGULATE INDUCTION OF MYOCARDIAL ORNITHINE DECARBOXYLASE IN MICE in vivo

JACK G. COPELAND, DOUGLAS F. LARSON, WILLIAM R. ROESKE, DIANE H. RUSSELL, J. R. WOMBLE

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

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. 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 μg/500 mg). Pretreatment with the β‐adrenoceptor antagonist, propranolol (10 mg/kg), totally blocked the increase in ODC activity. Elevation of myocardial ODC activity was not inhibited by metoprolol, a relatively specific β1‐adrenoceptor antagonist, at a dose of 10 mg/kg. Since the increase in ODC activity was blocked by a β‐adrenoceptor antagonist (propranolol) and enzyme activity was stimulated by terbutaline, a β2‐agonist, we conclude that β2‐adrenoceptors are selectively coupled to the regulation of murine cardiac ODC activity following catecholamine stimulation. 1982 British Pharmacological Society

Original languageEnglish (US)
Pages (from-to)479-483
Number of pages5
JournalBritish Journal of Pharmacology
Volume75
Issue number3
DOIs
StatePublished - Mar 1982

ASJC Scopus subject areas

  • Pharmacology

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