Effects of ranolazine on oxidative substrate preference in epitrochlearis muscle. McCormack, James G., Vickie E. Baracos, Rick Barr, and Gary D. Lopaschuk. Department of Pharmacology, Syntex Research Centre, Heriot-Watt University Research Park, Riccarton, Edinburgh, Scotland, UK, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Canada, Departments of Pediatrics and Pharmacology, 423 Heritage Medical Research Center, University of Alberta, Edmonton, Canada
APStracts 3:0160A, 1996.
Ranolazine is an novel investigational anti-anginal agent which stimulates glucose oxidation in isolated rat hearts. This study determined its effects on metabolic substrate and O2 utilization in an in vitro skeletal muscle preparation, the rat epitrochlearis muscle. Muscles were superfused with Krebs'-Henseleit buffer containing 3% albumin, 0.4mM palmitate, 5.5mM glucose, 0.5mM lactate and a physiological amino acid mixture. Perfusate also contained either (i) [U-14C]-glucose for measurement of glucose oxidation, or (ii) [9,10-3H]-palmitate and [U-14C]-lactate for measurement of palmitate and lactate oxidation. Addition of ranolazine (10 [mu]M) significantly stimulated glucose oxidation and decreased palmitate oxidation, but had no effect on lactate oxidation. Overall, the calculated relative contribution of glucose oxidation to aerobic ATP production increased from 12% to 33%, whereas from palmitate it decreased from 55% to 26%. Ranolazine did not alter tissue malonyl CoA contents, making it unlikely that the decrease in palmitate oxidation caused by ranolazine is due to a decrease in the activity of acetyl CoA carboxylase. These data demonstrate that ranolazine can shift energy substrate preference in skeletal muscle, which could potentially prove useful in ischemic disorders of skeletal muscle.

Received 28 September 1995; accepted in final form 14 March 1996.
APS Manuscript Number A1045-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96