Dec. 3, 1997 Like a car, the heart depends on a complex and tightly timed series of electrical and mechanical events to do its job. If its precisely synchronized system malfunctions, the car may stall–and the heart may suffer cardiac arrhythmias, life-threatening disruptions in the coordination of contractions in different regions of the heart muscle needed to keep blood pumping through the body. Arrhythmias kill nearly half a million Americans a year, and there is no effective drug therapy.
Just as the electrical system of a car triggers movement of the pistons, electrical events in the heart trigger its contraction. Now researchers at the University of Maryland School of Medicine have identified a previously unrecognized step in the electrical process of stimulating the heart to beat, a new sodium channel that could pave the way for effective drug treatments for cardiac arrhythmias.
C. William Balke, MD, associate professor of medicine and physiology; Lawrence Goldman, PhD, professor of physiology; Stephen R. Shorofsky, MD/PhD, assistant professor of medicine; and Rajesh Aggarwal, PhD, research associate in medicine, report their findings in the December 1, 1997 issue of the Journal of Physiology (London).
Balke describes the new sodium channel as "a seminal finding with broad implications, not just in the heart, but in many kinds of excitable cells."
A sodium channel is a minute pathway through the membrane or outer surface of cells. Made up of protein molecules embedded in the cell membrane of heart muscle cells, sodium channels open and close in response to electrochemical changes, allowing positively charged ions to pass into the cell and trigger the rhythmic contractions that pump blood through the body’s circulatory system. Electrophysiologists have known about sodium channels in heart muscle for some time. It had long been believed that the rhythmic electrical activity of the heart caused contraction by directly opening these "classical" sodium channels in heart muscle cells. Balke and Goldman found instead that the heart’s rhythmic electrical activity opens a new type of sodium channel, which in turn opens the classical sodium channels that trigger contraction of ventricular cells.
The new sodium channel appears to be a previously unknown and vital step in the normal sequence of electrical activity that causes the heart to pump. Balke calls it a "gatekeeper" between the electrical signal and contraction of heart muscle. "This may give us a tool for preventing and correcting arrhythmias," he said. "It is a trigger we didn’t know existed, and it gives us a whole new target for pharmacological therapy for arrhythmias." Added Goldman: "Even if it isn’t the source of the defect, if you can modulate it properly, you should be able to control the arrhythmia," The Maryland investigators’ research was funded in part by the National Institutes of Health.
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