Roderick, H. L.; Higazi, D. R.; Smyrnias, I.; Fearnley, C.; Harzheim, D. and Bootman, M. D.
|DOI (Digital Object Identifier) Link:||http://dx.doi.org/10.1042/BST0350957|
|Google Scholar:||Look up in Google Scholar|
Ca(2+) increases in the heart control both contraction and transcription. To accommodate a short-term increased cardiovascular demand, neurohormonal modulators acting on the cardiac pacemaker and individual myocytes induce an increase in frequency and magnitude of myocyte contraction respectively. Prolonged, enhanced function results in hypertrophic growth of the heart, which is initially also associated with greater Ca(2+) signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca(2+) signalling capacity and cardiac output are reduced. Here, the role that Ca(2+) plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca(2+) fluxes will be discussed.
|Item Type:||Journal Article|
|Copyright Holders:||2007 The Biochemical Society, The Authors|
|Academic Unit/Department:||Science > Life, Health and Chemical Sciences
|Interdisciplinary Research Centre:||Biomedical Research Network (BRN)|
|Depositing User:||Martin Bootman|
|Date Deposited:||25 Oct 2012 10:47|
|Last Modified:||18 Jan 2016 15:49|
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