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Am J Physiol Heart Circ Physiol 274: H8-H17, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 1, H8-H17, January 1998

Pyruvate augments calcium transients and cell shortening in rat ventricular myocytes

Bradley J. Martin, Hector H. Valdivia, Rolf Bünger, Robert D. Lasley, and Robert M. Mentzer Jr.

Division of Cardiothoracic Surgery, University of Wisconsin School of Medicine, Madison, Wisconsin 53792-0001; and Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799

Pyruvate has been shown to be a metabolic inotrope in the myocardium. In millimolar concentrations, it has been shown to increase both myocardial phosphorylation potential and the cytosolic [NAD+]-to-[NADH] ratio. To determine if changes in these parameters can alter intracellular Ca2+ concentration ([Ca2+]i) and hence contractile function, Ca2+ transients and cell shortening (CS) were measured in isolated rat ventricular myocytes superfused with a physiological N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffer (11 mmol/l glucose) with and without additional pyruvate, L-lactate, acetate, or isoproterenol. The addition of 5 mmol/l pyruvate resulted in a 33% increase in CS and a 39% increase in systolic [Ca2+]i. These pyruvate effects were 70% of those observed with 100 nmol/l isoproterenol. The mitochondrial monocarboxylate transport inhibitor alpha -cyano-4-hydroxycinnamate (250 µmol/l) strongly inhibited pyruvate inotropy, suggesting a substantial obligatory coupling between pyruvate inotropism and its oxidation by the mitochondria. A possible role of the cytosolic [NAD+]-to-[NADH] ratio was assessed by comparing the effects of 20 mmol/l L-lactate to those of equimolar pyruvate. In contrast to 20 mmol/l pyruvate, excess L-lactate failed to appreciably increase CS or systolic [Ca2+]i. The findings imply that, at levels substantially above 5 mmol/l, a portion of pyruvate inotropism might be due to extreme cytosolic [NAD+]-to-[NADH] ratios. This study is the first evidence that augmented [Ca2+]i transients are most likely the mechanism of cardiac pyruvate inotropism.

mitochondria; sarcoplasmic reticulum


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