Thyroid hormone regulation of cardiac bioenergetics: role of intracellular creatine.

Autor: Queiroz, Marcia Silva, Shao, Yvonne, Berkich, Deborah A., Lanoue, Kathryn F., Ismail-Beigi, Faramarz
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Zdroj: American Journal of Physiology: Heart & Circulatory Physiology; Dec2002, Vol. 283 Issue 6, pH2527, 7p, 2 Diagrams, 2 Charts, 8 Graphs
Abstrakt: The effect of thyroid hormone (T[sub 3]) on the content of myocardial creatine (Cr), Cr phosphate (CrP), and high-energy adenine nucleotides and on cardiac function was examined. In the hearts of control and T[sub 3]-treated rats perfused in vitro, while "low" and "high" contractile work was performed, T[sub 3] treatment resulted in a ∼50% reduction in CrP, Cr, total Cr content (Cr + CrP), and in the CrP-to-Cr ratio. In addition, there was a slight fall in myocardial content of ATP and a large rise in calculated free ADP (fADP), resulting in a significant decrease in the ATP-to-fADP ratio in the hearts of hyperthyroid compared with euthyroid rats. Moreover, there was a substantial decrease in the level of ATP in hearts of T[sub 3]-treated rats under high work conditions. Importantly, the ratio of cardiac work to oxygen consumption was not altered by thyroid status. Treatment with T[sub 3] also resulted in an almost threefold reduction in the content of Na[sup +]/Cr transporter mRNA in the ventricular myocardium and skeletal muscle but not in the brain. We conclude with the following: 1) changes in the expression of the Na[sup +]/Cr transporter mRNA correlate with Cr + CrP in the myocardium; 2) hearts of hyperthyroid rats contain lower levels of ATP and higher levels of fADP under both low and high work conditions but no reduction in efficiency of work output; and 3) the reduction in Cr and ATP in hearts of hyperthyroid rats may be the basis for the reduced maximal work capacity of the hyperthyroid heart. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index