The ultrarapid delayed rectifier current I(Kur) exhibits distinct molecular bases across species and tissues, representing a potential target for new antiarrhythmic drug development.
This review highlights the molecular diversity of cardiac ultrarapid delayed rectifier currents (I(Kur)) and their potential as targets for novel antiarrhythmic therapies.
Classical cardiac delayed rectifier currents activate at least two orders of magnitude slower than delayed rectifier currents in nerve and skeletal muscle tissue. It has recently become evident that many cardiac tissues express delayed rectifier currents with kinetics similar to those of nerve and muscle. These currents have been designated I(Kur) (for 'ultrarapid' delayed rectifier), in contrast to the classical cardiac rapid (I(Kr)) and slow (I(Ks)) delayed rectifier components. Although the kinetics of I(Kur) in different species and tissues are similar, their pharmacological properties vary greatly. It now appears that the differences among various I(Kur)s are due to differences in the molecular basis. A variety of Shaker-related clones (Kv1.2, 1.5, 2.1 and 3.1) that form I(Kur) channels upon heterologous expression have been identified with specific I(Kur)s (e.g. Kv1.2, rat atrium; Kv1.5, mouse ventricle and human atrium; Kv3.1, dog atrium). The present article reviews the distribution, biophysical and pharmacological properties, molecular basis and functional role of I(Kur), as well as the potential value of I(Kur) as a target for new antiarrhythmic drug development.
Nattel et al. (Fri,) conducted a review in Cardiac arrhythmias. I(Kur) channels was evaluated. The ultrarapid delayed rectifier current I(Kur) exhibits distinct molecular bases across species and tissues, representing a potential target for new antiarrhythmic drug development.