Abstract

Adenosine (Ado) is a naturally occurring compound that has several important cardiovascular actions, including activation of ATP-sensitive K(+) channels in vascular smooth muscle, vasorelaxation, and an effect to alter glucose metabolism of cardiac muscle. The metabolic effects of Ado on vascular smooth muscle have not been defined and were examined in this study. Porcine carotid artery strips were incubated in the presence and absence of 0.5 mM Ado. Compared with the control, Ado had no effect on glucose uptake, glucose oxidation, or fatty acid (octanoate) oxidation. Ado suppressed glycolysis but enhanced glycogen synthesis. Relative to the rate of glycolysis, Ado increased lactate production. Ado stimulated O(2) consumption by 52 +/- 10%, altered the activities of the tricarboxylic acid cycle and malate-aspartate shuttle, and increased the content of ATP, ADP, AMP, and phosphocreatine. Alteration in the metabolic variables by Ado could not be attributed to diminished energy requirements of reduced resting muscle tone of the arterial strips. Relaxation of the arterial strips in response to Ado were abolished in arteries incubated under hypoxic conditions (95% N(2)-5% CO(2)). Hypoxia was associated with increased ADP content. It is concluded that Ado affected glucose metabolism indirectly. The metabolic and energetic effects of 0.5 mM Ado are mediated by alterations in the concentrations of AMP, ATP, and phosphorylation potential (ATP/ADP).

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