Substrate dependent alteration in oxygen consumption and energy metabolism in contracting vascular smooth muscle. Barron, John T., Stephen J. Kopp, June Tow, and Joseph E. Parrillo. Section of Cardiology, Department of Medicine, Rush Medical College, Chicago, Illinois and 2Department of Physiology, Midwestern University, Downers Grove, Illinois
APStracts 2:0489H, 1995.
Energy metabolism and the substrate utilization pattern of intact porcine carotid artery was investigated in the presence or absence of glucose and/or octanoate during the phases of isometric contraction induced by K+- depolarization. During the early phase of contraction, there was a rapid increase in the rate of O2 uptake which was independent of the rate of force generation but dependent on the availability of intracellular pyruvate, the source of which was glucose and not glycogen. Lactate production increased linearly from the onset of contractile stimulation and was not suppressed by octanoate oxidation. There was no alteration from the basal resting state in the concentrations of the metabolites of the tricarboxylic acid cycle, either in the presence or absence of octanoate. During the phase of steady state force maintenance, O2 consumption was increased when compared with the basal unstimulated rate, but was not increased when both glucose and octanoate were present, consistent with the Crabtree effect. This was associated with increased aerobic lactic acid production and inhibition of the tricarboxylic acid cycle at the citrate synthase step. Alteration of the high energy phosphate content could not account for the pattern of O2 consumption during contraction under different substrate conditions. In the absence of glucose, the energy from octanoate oxidation could substitute for the energy ordinarily derived from aerobic glycogen and lactic acid production. It is concluded that energy metabolism of vascular smooth muscle is coordinated during contraction by feedback regulation and integration of the pathways of aerobic glycolysis and oxidative phosphorylation. 

Received 5 July 1995; accepted in final form 16 October 1995.
APS Manuscript Number H616-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95