REDUCTION BY BETA-ADRENOCEPTOR BLOCKADE OF HYPOXIA-INDUCED RIGHT HEART HYPERTROPHY IN THE RAT

1 The study was undertaken to assess the role of beta-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 i n haematocrit. 3 The hypoxia-induced right ventricular hypertrophic re sponse was reduced by 65% by oral treatment with a high dose of the no n-selective beta-adrenoceptor antagonist, propranolol (80 mg kg(-1) bo dy weight); the drug treatment caused only a minor reduction (6%) in s econdary polycythaemia. 4 With a less severe degree of hypoxia (7% ins pired oxygen) there was only minimal secondary polycythaemia (+ 15%), and a lesser degree of compensatory right ventricular hypertrophy in u ntreated rats (+33%). 5 Treatment with the beta(1)-adrenoceptor antago nist, atenolol, in a dose of 80 mg kg(-1) body weight abolished right ventricular hypertrophy in response to 7% inspired oxygen, without aff ecting haematocrit and caused a small reduction in the ratio of heart weight to body weight in normoxic rats. 6 The results show that the ef fect of propranolol on hypoxic right ventricular hypertrophy is not se condary to any effect on secondary polycythaemia as has previously bee n suggested and that a marked reduction of compensatory cardiac hypert rophy can be obtained by a beta(1)-selective adrenoceptor antagonist. Thus these findings support the view that noradrenaline released from cardiac sympathetic nerve terminals exerts a trophic effect on myocard ial cells and demonstrates that in vivo, this trophic effect can be re duced by beta(1)-adrenoceptor blockade.