Acetate transiently inhibits myocardial contraction by increasing mitochondrial calcium uptakeReport as inadecuate

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BMC Physiology

, 14:12

Circulation, cardiovascular and respiratory disease


BackgroundThere is a close relationship between cardiovascular disease and cardiac energy metabolism, and we have previously demonstrated that palmitate inhibits myocyte contraction by increasing Kv channel activity and decreasing the action potential duration. Glucose and long chain fatty acids are the major fuel sources supporting cardiac function; however, cardiac myocytes can utilize a variety of substrates for energy generation, and previous studies demonstrate the acetate is rapidly taken up and oxidized by the heart. In this study, we tested the effects of acetate on contractile function of isolated mouse ventricular myocytes.

ResultsAcute exposure of myocytes to 10 mM sodium acetate caused a marked, but transient, decrease in systolic sarcomere shortening 1.49 ± 0.20% vs. 5.58 ± 0.49% in control, accompanied by a significant increase in diastolic sarcomere length 1.81 ± 0.01 μm vs. 1.77 ± 0.01 μm in control, with a near linear dose response in the 1–10 mM range. Unlike palmitate, acetate caused no change in action potential duration; however, acetate markedly increased mitochondrial Ca uptake. Moreover, pretreatment of cells with the mitochondrial Ca uptake blocker, Ru-360 10 μM, markedly suppressed the effect of acetate on contraction.

ConclusionsLehninger and others have previously demonstrated that the anions of weak aliphatic acids such as acetate stimulate Ca uptake in isolated mitochondria. Here we show that this effect of acetate appears to extend to isolated cardiac myocytes where it transiently modulates cell contraction.

Electronic supplementary materialThe online version of this article doi:10.1186-s12899-014-0012-2 contains supplementary material, which is available to authorized users.

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Author: James F Schooley - Aryan MA Namboodiri - Rachel T Cox - Rolf Bünger - Thomas P Flagg


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