Abstract

The effect of metabolic inhibitors on myogenic tone, norepinephrine and barium chlorideinduced contractions, adenosine triphosphate (ATP) content, ⁴⁵Ca uptake and efflux and the total calcium content of tibial arteries were evaluated with the technique of superfusion in the absence and presence of ruthenium red, dinitrophenol, cyanide, azide and fluoroacetate. Ruthenium red did not affect myogenic tone despite a decrease in passive ⁴⁵Ca influx. Each of the remaining metabolic inhibitors decreased myogenic tone and ATP despite an increase in ⁴⁵Ca influx and total tibial artery calcium content. Dinitrophenol reduced slightly the contractile responses of tibial arteries to norepinephrine and almost abolished the contractile response to barium chloride. Cyanide, azide and fluoroacetic acid did not significantly alter the contractile responses of tibial arteries to norepinephrine or barium chloride. These data are consistent with the conclusions that myogenic tone and norepinephrine-induced contraction can be differentially inhibited by inhibition of metabolism and calcium uptake. Inhibitors of oxidative metabolism decreased myogenic tone with little inhibition of the responses to vasoactive stimuli. These data suggest that myogenic tone is in some manner dependent on a functional tricarboxylic acid cycle and oxidative phosphorylation. Inhibition of resting calcium influx did not affect myogenic tone. Therefore, myogenic tone does not appear to be primarily dependent on the fraction of passive calcium influx inhibited by ruthenium red. In addition, the ability of ATP-deficient, metabolically inhibited tibial arteries to contract to norepinephrine and barium chloride suggests that energy for norepinephrine and barium chloride-induced contractions do not appear to be dependent on preformed existing stores of ATP generated via the tricarboxylic acid cycle and oxidative phosphorylation or that a large safety factor exists for maintaining contractile integrity of this preparation.