New insight into the heartbeat (9/9/2007)

Scientists may develop a better understanding of cardiac function in health and disease by using a new way to look at key proteins that activate heart muscle contraction.

Researchers at The University of Auckland have conducted studies on ventricular heart muscle cells, including developing novel optical methods for tracing proteins that play a major role in activating cardiac contraction. The research, lead by Dr Christian Soeller and Professor Mark Cannell from the Faculty of Medical and Health Sciences, is published in this week’s Early Edition of the prestigious US journal Proceedings of the National Academy of Science.

With every beat, weak electrical currents travel through the heart and, via a chain of events at the molecular scale, cause specialised receptors called ‘ryanodine receptors’ to release minute amounts of calcium into the cell interior. This leads to a concerted contraction that pushes blood around the body with every heart beat.

By combining advanced optical and computer processing methods, the new research has developed a novel way of visualising and quantifying these proteins with three-dimensional resolution, the first of its kind for human heart cells. While the work focused on visualising the receptor distribution in healthy cells, the new techniques are ideally suited to look for changes that occur when cardiac muscle is diseased or damaged.

"Understanding the pathways that control contraction is vital to improving our understanding of how the heart works and how we can treat it when problems arise," says Dr Christian Soeller. "Through our studies, we now have a way of determining the distribution of receptors central to cardiac contraction with ultrahigh three-dimensional resolution."

Key to the efficient pumping of blood throughout the circulation is the rythmic near-simultaneous contraction of all muscle cells in the heart. Evidence from international research is mounting that changes in the pattern in which ryanodine receptors are activated in individual heart cells may give rise to poorly synchronised contractions called ‘arrythmias’. Even very subtle changes in the distribution of the ryanodine receptors may make the heart more prone to experience such periods of potentially life threatening arrythmias.

"The new approaches that we have developed provide very sensitive tools to test if such structural changes are implicated in some of the problems that patients with certain heart conditions experience," adds Professor Mark Cannell.

Further work to extend the current work to study the structure of heart cells from patients with failing hearts is currently under way in Dr. Soeller’s and Professor Cannell’s laboratory.

The research was supported by grants from the Auckland Medical Research Foundation and a Programme from the Health Research Council of New Zealand.

Note: This story has been adapted from a news release issued by The University of Auckland

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