Effects of Hyperthyroidism on Contractility and Na+/Ca2+ Exchanger Activity in the Isolated Papillary Muscle of Rats

Abstract

The thyroid hormones (TH) play a role in the entire organism, regulating biological processes, such as metabolic rate, oxygen consumption, gene transcription, and protein synthesis. 1,2 Hyperthyroidism (Hy) is characterized by an increase in the endogenous production of the triiodothyronine (T3) and/or thyroxine (T4) hormones, or by the exogenous administration of these hormones. 3 The heart is the major target organ for TH actions. 4,5 In the heart, TH has an effect on the membrane ion channels, 6 on the contractile apparatus, and on the sarcoplasmic reticulum (SR), 7 which are linked to the excitation-contraction coupling mechanism 8 and directly alter contractility. 9 Common changes reported in the hyperthyroid heart are increased myocardial contractility and cardiac output, 2 improvement in diastolic relaxation, 10 changes in electrical activity, 7 increments in ventricular mass, 5 and arrhythmias. 1

Hyperthyroidism and Cardiac Contractility

“…In this Journal, the authors study, in rat models, the intracellular mechanisms involved in the excess of thyroid hormones (hyperthyroidism) in the contractility and Na+/Ca2+ Exchanger Activity in the heart muscle. 3 However, not all physiological mechanisms can be extrapolated from animals to humans because of their differences and specificities. In clinical practice, we still control heart rate with beta-blockers, and in case of contraindication, with benzothiazepine and calcium channel blocker.…”