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β 2 ‐ADRENOCEPTORS REGULATE INDUCTION OF MYOCARDIAL ORNITHINE DECARBOXYLASE IN MICE in vivo
Author(s) -
COPELAND JACK G.,
LARSON DOUGLAS F.,
ROESKE WILLIAM R.,
RUSSELL DIANE H.,
WOMBLE J.R.
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb09164.x
Subject(s) - isoprenaline , ornithine decarboxylase , terbutaline , endocrinology , medicine , propranolol , antagonist , fenoterol , in vivo , chemistry , metoprolol , agonist , stimulation , biology , enzyme , receptor , biochemistry , microbiology and biotechnology , asthma
1 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 μg/500 mg). 3 Pretreatment with the β‐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 β 1 ‐adrenoceptor antagonist, at a dose of 10 mg/kg. 5 Since the increase in ODC activity was blocked by a β‐adrenoceptor antagonist (propranolol) and enzyme activity was stimulated by terbutaline, a β 2 ‐agonist, we conclude that β 2 ‐adrenoceptors are selectively coupled to the regulation of murine cardiac ODC activity following catecholamine stimulation.

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