Increased cardiac workload by closure of the ductus arteriosus leads to hypertrophy and apoptosis rather than to hyperplasia in the late fetal period

Naunyn-Schmiedeberg's Archives of Pharmacology
M J van den HoffA F Moorman

Abstract

It is generally thought that adult mammalian cardiomyocytes compensate for an increased workload by hypertrophy, whereas fetal myocardium grows by cellular proliferation. We analyzed the response of late-fetal rat hearts upon an increased workload imposed by premature constriction of the ductus arteriosus with indomethacin. Initially the fetal heart responds by proliferative growth, as both wet weight and labeling index (bromodeoxyuridine incorporation) of the ventricles increased, whereas neither a change in the fibroblast fraction, ploidy and nucleation in the ventricles is observed. However, this hyperplastic growth is abrogated by a subsequent burst in apoptosis and followed by a hypertrophic response as based on a decrease in DNA and increase in both RNA and protein concentration. This hypertrophic growth was accompanied by a 1.4-fold increase in the volume of the cardiomyocytes. Changes in the molecular phenotype characteristic of pressure-overload hypertrophic growth accompany the process. Thus, the levels of expression of beta-myosin heavy chain and atrial natriuretic factor mRNA increased, of sarcoplasmic/endoplasmic reticulum ATPase (SERCA2) mRNA decreased, and of alpha-myosin heavy chain, phospholamban, and calseques...Continue Reading

Citations

Feb 9, 2010·Expert Review of Cardiovascular Therapy·Paulo ZielinskyLuiz Henrique Soares Nicoloso
Jan 14, 2009·International Journal of Cardiology·Olga V AnatskayaAlexander E Vinogradov
Dec 18, 2013·Birth Defects Research. Part C, Embryo Today : Reviews·Paulo Zielinsky, Stefano Busato
Apr 18, 2006·American Journal of Physiology. Heart and Circulatory Physiology·Kimimasa TobitaBradley B Keller

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