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Reduction by β‐adrenoceptor blockade of hypoxia‐induced right heart hypertrophy in the rat
Author(s) -
ÖstmanSmith I.
Publication year - 1995
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.1476-5381.1995.tb17229.x
Subject(s) - medicine , propranolol , polycythaemia , muscle hypertrophy , hypoxia (environmental) , right ventricular hypertrophy , endocrinology , atenolol , antagonist , chemistry , blood pressure , oxygen , receptor , ventricle , organic chemistry
1 The study was undertaken to assess the role of β‐adrenoceptors in the induction of compensatory cardiac hypertrophy in an in vivo model. 2 In the rat, exposure to severe hypoxia (6% inspired oxygen for 8 h day) caused a 51% increase in right heart weight and a 75% increase in haematocrit. 3 The hypoxia‐induced right ventricular hypertrophic response was reduced by 65% by oral treatment with a high dose of the non‐selective β‐adrenoceptor antagonist, propranolol (80 mg kg −1 body weight); the drug treatment caused only a minor reduction (6%) in secondary polycythaemia. 4 With a less severe degree of hypoxia (7% inspired oxygen) there was only minimal secondary polycythaemia (+ 15%), and a lesser degree of compensatory right ventricular hypertrophy in untreated rats (+ 33%). 5 Treatment with the β 1 ‐adrenoceptor antagonist, atenolol, in a dose of 80 mg kg −1 body weight abolished right ventricular hypertrophy in response to 7% inspired oxygen, without affecting haematocrit and caused a small reduction in the ratio of heart weight to body weight in normoxic rats. 6 The results show that the effect of propranolol on hypoxic right ventricular hypertrophy is not secondary to any effect on secondary polycythaemia as has previously been suggested and that a marked reduction of compensatory cardiac hypertrophy can be obtained by a β 1 ‐selective adrenoceptor antagonist. Thus these findings support the view that noradrenaline released from cardiac sympathetic nerve terminals exerts a trophic effect on myocardial cells and demonstrates that in vivo , this trophic effect can be reduced by β 1 ‐adrenoceptor blockade.