Thyroid-induced alterations in myocardial sodium-potassium-activated adenosine triphosphatase, monovalent cation active transport, and cardiac glycoside binding.

Abstract

A B S T R A C TrThe effects of thyroid hormn-one on guinea pig imiyocardial NaK-ATPase activity, transmemnbranie imion-ovalenit cationi active transport, and cardliae glycosi(le binlding were examined. NaKATPase activities of left atrial anid left ventricular homiogeniates of control and triiodothyronine (T3)-treated animiials were determinecl, and compared to activities of skeletal mluisele and( liver. T3 administrationi was associated withl a significanit increase of 18% in left atrial and left ventricular NaK-ATPase specific activities. This increment was less than that notedI in skeletal mltusele (+42%) and liver (+30%). To (letermiinle if enhanicedl NaK-ATPase activity was accomiipanied by increased monovalent cation active tranisport, in vitro 86Rb+ uptake by left atrial strips and hemiidliaplhragmiis was measured. Transition from the euthyroid to the hyperthyroid state resulted in a 68% increase in active 86Rb+tuptake by left atrium, and a 62% increase in active uiptake by (liaphragm. Passive 86Rb+ uiptake was nlot affected in either tissue.Ouabain binding by atrial and ventricular homogeniates of T3-treated animials was increased by 19 and 17%, respectively, comppared to controls, in close agreemiient with thyroid-induced increments in NaKATPase activity. Taken together, these results are consistenit with enhanced myocardial NaK-ATPase activity and imonovalent cation active transport due to an increase in the number of finctional enzyme complexes.

Thyroidal enhancement of rat myocardial Na,K-ATPase: Preferential expression of α2 activity and mRNA abundance

“…Thyroid hormone (T3) stimulates the Na,KATPase activity of a variety of mammalian target tissues [2,8,16,22,33]. The enhancement of Na,KATPase activity by T3 is associated with increased numbers of specific ouabain-binding of Na+-dependent phosphorylation sites in plasma membranes isolated from target tissues [21,22].…”

Effect of thyroid hormone on slow calcium channel function in cultured chick ventricular cells.

“…These findings have led to the hypothesis that enhancement of myocardial contractility by thyroid hormones is the result of increased cardiac myosin ATPase ac-tivity. However, thyroid hormone has also been reported to alter Ca uptake by sarcoplasmic reticulum (9)(10)(11)(12)(13)(14), to stimulate plasma membrane Ca-ATPase activity (4,15,16), and also to increase the numbers of sarcolemmal sodium pump sites (17)(18)(19). Therefore, the mechanisms by which myocardial contractility is enhanced in response to thyroid hormone appear to include altered Ca handling by sarcoplasmic reticulum and also changes in sarcolemmal membrane function that would directly influence the excitation-contraction coupling process.…”

Effects of thyroid hormone on sodium pump sites, sodium content, and contractile responses to cardiac glycosides in cultured chick ventricular cells.

“…At the cellular level, thyroid hormone has been shown to increase NaK-ATPase activity (9-1 1) and the number of NaKATPase complexes in several types of tissues (12)(13)(14)(15). If other properties of myocardial cells remained constant, we would expect such changes in the number of sodium pump sites or sodium pump activity to alter intracellular sodium content, and hence, sodium-calcium exchange across sarcolemmal membranes (16)(17)(18)(19).…”