@article{APS6302,
author = {Lai-jing Song and Guan-lei Wang and Jie Liu and Qin-ying Qiu and Jing-hua Ou and Yong-yuan Guan},
title = {Cellular mechanisms of reduced sarcoplasmic reticulum Ca 2+ content in L -thyroxin-induced rat ventricular hypertrophy},
journal = {Acta Pharmacologica Sinica},
volume = {29},
number = {4},
year = {2016},
keywords = {},
abstract = {Aim: To examine how the sarcoplasmic reticulum (SR) Ca2+ content changes and the underlying mechanism in L-thyroxin-induced cardiac hypertrophy.
Methods: Echocardiography was used to confirm the establishment of the cardiac hypertrophy model. The confocal microscopy and fluorescent indicator Fluo-3 was applied to examine the intracellular Ca2+ concentration ([Ca2+]i), the Ca2+ sparks, and the caffeine-induced Ca2+ transient in freshly isolated cardiac ventricular myocytes. The activity of sarcolemmal and SR Ca2+-ATPase 2a (SERCA2a) in the ventricular tissue was also measured, respectively.
Results: L-thyroxin (1 mg/kg injection for 10 d) induces left ventricular cardiac hypertrophy with normal myocardial function. The decreased caffeine-induced Ca2+ transient in the Ca2+-free solution was detected. The spontaneous Ca2+ sparks in hypertrophied myocytes occurred more frequently than in normal cells, with similar duration and spatial spread, but smaller amplitude. Then the basal [Ca2+]i increase was observed in quiescent left ventricular myocytes from hyperthyroidism rats. The activity of sarcolemmal and SR Ca2+-ATPase was decreased in the hypertrophied ventricle tissue.
Conclusion: The results suggested that the reduced SR Ca2+ content may be associated with an increased Ca2+ leak and reduced SERCA2a activity, contributing to abnormal intracellular Ca2+ handling during hypertrophy in hyperthyroidism rats.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/6302}
}