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February 14, 2012--------News Archive Return to: News Alerts


Molecular model showing the interaction between the sodium channel ‘plug’
that helps regulate heart rate - and the calmodulin protein (red) that regulates it.

White markings at top are the ECG traces
(left: Brugada syndrome arrhythmia; right: normal)
Courtesy of: F. van Petegem, UBC.

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The Link Between Sodium, Calcium and Heartbeat

That flutter in your heart may have more to do with the movement of sodium ions than the glance of a certain someone across a crowded room

Researchers from the University of British Columbia (UBC) have revealed for the first time, one of the molecular mechanisms that regulates the beating of heart cells by controlling the movement of sodium through the cell wall.

The findings, published February 14 in the Proceedings of the National Academy of Sciences, sheds new light on this crucial physiological process while revealing the root cause and possible treatment targets of two potentially life-threatening cardiac arrhythmia conditions.

The contraction and relaxation of heart muscle cells depend on minute, but finely regulated electrical impulses. These impulses are created when charged atoms (or ions) of metals such as sodium, potassium and calcium, pass between cells. Irregular heartbeats, arrhythmias, can happen when the transfer of these ions leak or a malfunction occurs.

Professors Filip van Petegem and Christopher Ahern, of UBC's Cardiovascular Research Group, used the Canadian Light Source Synchrotron (CLS) to determine the molecular structure controlling the flow of sodium to the heart, and to other electrically-excitable cells in the nervous system.

"The heart is an electrical organ that depends on precise electrical signals to contract [and pump blood]" explains van Petegem. "It is crucial for heart rate that the signalling, controlled by the movement of sodium, be exact. So the entry of sodium into the cell is tightly regulated."

The sodium channel controlling access through the outer membrane of a heart cell, is a huge, intertwined four-part molecule. Van Petegem and Ahern examined a section of that molecule where a plug forms to stop sodium from entering the cell.

They discovered a protein, calmodulin, binding to the sodium channel, preventing the plug from forming and forcing the channel open. Problems occur with this system when genetic mutations change the shape of the channel at the protein binding site, affecting how well the channel can open and close. When flow of sodium into the muscle cells is disrupted, the heart does not beat in rthym.

The scientists were able to identify mutations in the site leading to two different kinds of heart arrhythmia: Brugada Syndrome and Long Q-T type 3. Brugada syndrome is considered to be caused by not enough sodium, while long Q-T is the result of too much sodium.

The results of the study could pave the way for the development of new drugs that can shore up how the calmodulin protein binds to the sodium channel, effectively treating both conditions and other arrhythmias.

"It's really a very elegant mechanism," notes van Petegem. "Many channels are regulated by calmodulin but not in such a simple way."

About the Canadian Light Source: The Canadian Light Source is Canada's national centre for synchrotron research and is a global leader and a recognized centre of excellence in synchrotron science and its applications. Located on the University of Saskatchewan campus in Saskatoon, the CLS has hosted over 4,600 user visits from academic institutions, government, and industry, and delivered over 15,000 experimental shifts to users from across Canada and 18 countries since 2005. CLS operations are funded by Western Economic Diversification Canada, Natural Sciences and Engineering Research Council, National Research Council of Canada, Canadian Institutes of Health Research, the Government of Saskatchewan and the University of Saskatchewan.www.lightsource.ca/media/quickfacts.php.

Original article: http://www.lightsource.ca/media/na-cahighlight.php