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AJP - Cell Physiology, Vol 244, Issue 5 385-C390, Copyright © 1983 by American Physiological Society
ARTICLES |
J. M. Krisanda and R. J. Paul
Previous studies (Paul, R. J. Chemical energetics of vascular smooth muscle. In: Handbook of Physiology: The Cardiovascular System. Bethesda, MD: Am. Physiol. Soc., 1980, p. 201-235) have shown that vascular oxygen consumption reaches a steady state at approximately twice the basal rate during maintenance of isometric contraction. The time course of the attainment of a metabolic steady state, the metabolic signal for the observed increase in respiration, and the contribution of endogenous phosphagens to the energetics of isometric contraction are not known with certainty. To this end, the time course of the tissue content of ATP, ADP, AMP, phosphocreatine (PCr), inorganic phosphate (Pi), and lactate were measured during a KCl-induced isometric contraction in porcine carotid artery and compared with values in the basal state. Oxygenated unpoisoned strips were frozen at 0, 0.5, 1, and 15 min of contraction, and tissue extracts were analyzed using analytical isotachophoresis. No statistically significant changes from the basal levels of ATP and PCr were measured. A small but significant increase in ADP was seen at all times. An increase in Pi of 1.25 mumol/g was observed at 0.5 min, which decreased in time. Tissue lactate content increased by 1.79 mumol/g after 1 min of contraction. The calculated range of cellular free ADP (ADPfree), 44-123 microM, may be sufficient to saturate oxidative phosphorylation. This and the apparent lack of change of ADPfree from basal during contraction suggest that it does not play a role in the coordination of metabolism and contractility. From as early as 0.5 min, when less than 40% of peak isometric force is attained, intermediary metabolism provides the total ATP required for contraction.
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