Abstract

1. The effects of propranolol, acebutolol and practolol on rat heart mitochondrial respiration and oxidative phosphorylation were examined. 2. Propranolol (0.2–0.5 mM) produced dose dependent decreases in state 3 oxygen consumption ( QO 2(3)), respiratory control index (RCI), ADP: O ratio and phosphorylation rate (PR) and increased state 4 oxygen consumption ( QO 2(4)). 3. The effects of propranolol were apparent regardless of the substrate used and were not reversed by the addition of 10–100 μM adrenaline. 4. Changes in mitochondrial activities due to acebutolol or practolol were observed only at high (3 mM) drug concentrations and the effects were qualitatively similar to those induced by propranolol. 5. The data support a possible role for drug-induced mitochondrial alterations, independent of β-blockade, in the negative inotropic action of propranolol.

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