Thyroid control over membrane processes in rat heart

¹ Laboratory of Hormonal Regulation, Tartu University, 202400 Tartu, Estonia; Laboratory of Bioenergetics, Institute of Experimental Cardiology, Cardiology Research Center of the USSR, 121552 Moscow, USSR; and Division of Cardiovascular Sciences, St. Boniface General Hospital Research Center and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada

We have studied the effects of hypo- and hyperthyroidism on sarcolemmal (SL) and sarcoplasmic reticular (SR) ion transport processes and mitochondrial energy production in rat heart. The following conclusions were derived. 1) Compared with euthyroid state, hyperthyroidism led to increased SR Ca²⁺-accumulation. In SL, the activities of Ca²⁺-stimulated adenosine triphosphatase (ATPase), ATP-dependent Ca²⁺ pumping, and Na⁺-Ca²⁺ exchanger were not affected; but ouabain-sensitive Na⁺-K⁺-ATPase activity was enhanced. 2) Hypothyroidism resulted in depressed activities of Ca²⁺ pumps both in SL and SR. In SL, the Na⁺-K⁺-ATPase activity was decreased, but Na⁺-Ca²⁺ exchange was unaltered. 3) Thus slower relaxation of the hypothyroid myocardium may be attributed to depressed functioning of Ca²⁺ pumps in SR and SL, whereas faster relaxation of the hyperthyroid heart may be based on increased Ca²⁺-pumping activity of SR. 4) Hyperthyroidism and hypothyroidism, respectively, led to enhanced and decreased rates of mitochondrial phosphocreatine synthesis. The thyroid state appears to control the functional coupling between mitochondrial creatine kinase and ATP-ADP translocase: the energy of oxidative phosphorylation was transformed into phosphocreatine more effectively in mitochondria from hypothyroid hearts than in those from hyperthyroid hearts.