An Atomic View Of The Trigger For The Heartbeat
Arthur T Knackerbracket has found the following story:
Atomic-level studies of the architecture of tiny sodium channel proteins, critical to generating electrical signals that start off each beat of the heart, are imparting striking details about their function, malfunctions, disruption by many disease mutations, and response to medication.
This structural information could become the basis for developing better diagnostics and drugs for life-threatening heart rhythm problems, according to the researchers from the University of Washington School of Medicine working in this area.
Their latest findings appear Dec. 19 in Cell in the paper, "Structure of the Cardiac Sodium Channel." The senior authors are William Catterall and Ning Zheng, both UW School of Medicine professors of pharmacology. The first authors are Daohau Jiang and Hui Shi, UW postdoctoral fellows in pharmacology.
"The cardiac sodium channel not only initiates the heartbeat, mutations in it also cause deadly arrhythmias, and antiarrhythmic drugs act directly on it to control cardiac rhythms," explained Catterall.
The heart is both a plumbing and electrical marvel. For each heartbeat, electrical waves travel across a healthy heart in a pattern that controls its filling and pumping in a tightly coordinated manner. The rate at which the impulse is propagated through the heart tissue relies on actions taking place at the molecular level in tiny protein pores present in cardiac cell membranes.
[...] The activation and quick inactivation of these voltage-gated sodium channels are part of a series of electrical and physiological events that maintain a steady heartbeat. "Sodium channels operate in concert with calcium channels and potassium channels to drive the heartbeat at a consistent frequency for our entire lives," Zheng noted.
When sodium channels don't work properly, the heart can be in trouble, even to the point of having dangerously fast and uncoordinated contractions that are life-threatening, the researchers explained.
Specifically, the NaV (Latin abbreviation for sodium, V for voltage) 1.5 channel has such an indispensable role that certain mutations in those channels can be fatal, because other sodium channels in the heart cannot compensate for their loss. These mutations can cause dangerous arrhythmias in adults and even sudden death in children and young athletes.
Journal Reference:
Daohua Jiang, Hui Shi, Lige Tonggu, Tamer M. Gamal El-Din, Michael J. Lenaeus, Yan Zhao, Craig Yoshioka, Ning Zheng, William A. Catterall. Structure of the Cardiac Sodium Channel. Cell, 2019; DOI: 10.1016/j.cell.2019.11.041
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