Thomas J. Hund, Ph.D., post-doctoral researcher in Pathology ( in Dr. Jeffrey Saffitz laboratory) at the Washington University School of Medicine, and Yoram Rudy, The Fred Saigh Distinguished Professor of Engineering at Washington University, have incorporated the Calcium/Calmodulin-dependent Protein Kinase II (CaMKII) regulatory pathway into their model, improving the understanding of the relationship between calcium handling in cardiac cells and the cell's electrical activity.

Normal contraction of the heart relies on normal generation of electrical signals, called action potentials, and their organized spread through cardiac tissue. The normal conduction of action potentials is reliant upon sodium channels. But slow conduction of action potentials that can lead to heart arrhythmias depends on calcium channels, which, in turn, are modulated by cell calcium.

" CaMKII mediates an important regulatory pathway that influences calcium cycling in the cell and modulates many processes involving calcium, including activities of calcium channels" said Rudy. "Having this pathway modeled is a valuable research tool because there is a strong link between abnormalities of calcium handling and cardiac arrhythmias. In addition, being a first mathematical model of a regulatory pathway involved in cell electrophysiology, it can serve as a paradigm for modeling effects of other regulatory pathways on cell function."

Rudy and Hund published their findings in the Nov. 16, 2004 issue of Circulation, a journal of the American Heart Association. The work was funded by grants from the National Institutes of Health - National Heart, Lung, and Blood Institute, and a Whitaker Foundation Development Awa
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Contact: Tony Fitzpatrick
tony_fitzpatrick@wustl.edu
314-935-5272
Washington University in St. Louis
8-Feb-2005