Excessive thyroxine enhances susceptibility to apoptosis and decreases contractility of cardiomyocytes

Molecular and Cellular Endocrinology
Yun-Ying WangZhi-Bin Yu

Abstract

Excessive thyroid hormone induces cardiac hypertrophy and promotes heart failure in patients with hyperthyroidism, but the mechanism remains elusive. Rats were orally administered with levothyroxine (100 microg/kg, T(4)) for 4 weeks to induce hyperthyroidism. The calculated stroke volume decreased and the shortening amplitude-frequency relationship in unloaded contraction of isolated cardiomyocytes was negative in T(4)-treated rats. Apoptotic rates increased and DNA laddering was also detectable in T(4)-treated rat hearts. By contrast, in primary cultured cardiomyocytes, T(3) induced dose-dependent hypertrophy but did not affect the apoptotic rate. Angiotensin II further increased the apoptotic rate of T(3)-induced hypertrophied cardiomyocytes. The apoptotic rate was dependent on the extent of cardiomyocyte hypertrophy. These results suggest that cardiac contractility is enhanced during the early stage of hyperthyroidism, but decreased during the late stage of hyperthyroidism. The hypertrophied cardiomyocytes were also susceptible to apoptotic stimulation by angiotensin II. Depressed cardiac contractility and enhanced apoptosis may lead to heart failure in hypertrophied myocardium.

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Citations

Jun 5, 2013·Apoptosis : an International Journal on Programmed Cell Death·M L Barreiro ArcosG A Cremaschi
Jun 1, 2012·TheScientificWorldJournal·Pallavi Mishra, Luna Samanta
Mar 21, 2013·Microcirculation : the Official Journal of the Microcirculatory Society, Inc·Felipe FreitasEduardo Tibiriçá
Aug 19, 2014·Clinical and Experimental Pharmacology & Physiology·Juan-Juan ShengZhi-Bin Yu
Oct 10, 2013·BioMed Research International·Lucia Oliveros-RuizJ Antonio G Hermosillo
Jul 7, 2015·Oxidative Medicine and Cellular Longevity·Mohammad T ElnakishPaul M L Janssen
Nov 8, 2017·Journal of Cardiovascular Pharmacology·Steven J RepasMohammad T Elnakish

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