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Journal of Pharmacology And Experimental Therapeutics, Vol. 182, Issue 2, 246-255, 1972
Copyright © 1972 by American Society for Pharmacology and Experimental Therapeutics


THE EFFECTS OF NOREPINEPHRINE AND PROPRANOLOL ON MYOCARDIAL SUBCELLULAR DISTRIBUTION OF TRIGLYCERIDES AND FREE FATTY ACIDS

T. N. MASTERS 1 and V. V. GLAVIANO 1

1 Department of Physiology, Loyola University Stritch School of Medicine, Maywood, Illinois

Myocardial subcellular alterations in free fatty acids (FFA) and triglycerides (TGFA) were measured in left ventricular muscle from open-chest mongrel dogs after the administration of propranolol (1 mg/kg i.v.) and norepinephrine (NE, 0.2 µg/kg/min i.v.). In one group of experiments (grup I) FFA and TGFA levels were determined in nuclear, mitochondrial, microsomal and supernatant fractions in control dogs and in dogs after the administration of NE or propranolol. In this group of experiments, propranolol elevated the TGFA concentration in mitochondrial, microsomal and supernatant fractions from control whereas the levels of FFA in the same fractions declined, with the most significant changes occurring in the supernant fraction. These results confirmed earlier reports from this laboratoy that propranolol may block myocardial FFA uptake by inhibiting intracellular TGFA degradation. NE was found to have no significant effect on the level (pool size) of FFA and TGFA in subcellular fractions of the myocardial muscle cell. In anoher group of experiments (group II), Na-palmitate-1-14C (50 µc) was infused into the left circumflex coronary artery of dogs treated wih proprnol or NE. Subcellular fractions were isolated and radioactivity of FFA, TGFA and phospholipids from these fractions was determined by liquid scintillation. Propranolol significantly increased activity of TGFA in the mitochondrial, microsomal and supernatant fractions which confirmed the inhibition of TGFA degradation found in group I with propranolol. However, NE increased the activity of TGFA in the mitochondrial, microsomal and supernatant fractions, indicating that the turnover of FFA through the TGFA moiety was increased, whereas its total intracellular level remained unchanged as observed in group I experiments. In response to both propranolol and NE, radioactivity in the FFA pool was reduced only in the supernatant fractions whereas little change was observed in phospholipid activity. The results of these experiments support the hypothesis that subcellular fractions containing pools of TGFA may have a role, especially in the supernatant fraction, in determining the myocardial uptake of FFA from arterial blood entering the heart.

Submitted on August 3, 1971
Accepted on April 23, 1972




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Copyright © 1972 by the American Society for Pharmacology and Experimental Therapeutics.