Effect of in vivo propranolol treatment on oxidative energy metabolism in rat liver and kidney mitochondria.

In vivo treatments with propranolol inhibited state 3 respiration in rat liver mitochondria with glutamate, pyruvate+malate, beta-hydroxybutyrate and succinate as substrates. The extent of inhibition was generally higher for the acute treatment. In the kidney mitochondria, the extent of inhibition of state 3 respiration for glutamate, pyruvate+malate and ascorbate+TMPD was equal in both acute and chronic treatments. However, the contents of cytochromes in both liver and kidney mitochondria remained unaffected by either of the drug treatments. The results suggest that prolonged use of the drug can have toxic effects on the respiratory activity of mitochondria even in the peripheral tissues, in addition to the target tissues.