Why the study?
Does zatebradine inhibit human cardiac K+ delayed rectifier currents (hKv1.5) in transfected Ltk- cells?
Population
Ltk- cells transfected with cloned human cardiac K+ delayed rectifier currents (hKv1.5) coding sequence
Comparison
Zatebradine (e.g., 10 mumol/L) vs Control (absence of drug)
Design
Preclinical
Authors
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May explain experimental APD prolongation; leaves open clinical translation or antiarrhythmic utility in humans.
Does zatebradine inhibit human cardiac K+ delayed rectifier currents (hKv1.5) in transfected Ltk- cells?
Zatebradine acts as an open-channel blocker of human cardiac K+ delayed rectifier currents (hKv1.5), providing a mechanistic explanation for its prolongation of the cardiac action potential.
Valenzuela et al. (1996) studied this question.
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