Title: Cardiac potassium channels in health and disease.

Authors: A M Brown

Journal, date & volume: Trends Cardiovasc. Med., 1997 May , 7, 118-24

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21235874

Abstract
Cardiac K(+)currents regulate resting membrane potential and action potential duration. These tasks are accomplished for the most part by four membrane currents: an inwardly rectifying current (I(K1)), a transient outward current (I(To)), and rapid (I(Kr)), and slow (I(Ks)) delayed rectifier currents. Recent studies have revealed far greater complexity at the molecular level. I(K1) may be produced by at least three genes from the Kir 2 subfamily of the supergene Kir family. The remaining currents appear to be produced by the supergene Kvα family, sometimes in association with the cytoplasmic protein Kvβ family. I(To) may be produced by the Kv4 subfamily, but members of the Kv1 subfamily could contribute, particularly if associated with Kvβ genes. Very rapid currents could be produced by Kv1.5, but Kvs 1.2 and 2.1 might also participate. Additional levels of complexity are possible because members within a Kv subfamily may form heterotetramers, and these, in turn, may associate with different Kvβs. The situation may be simpler for I(Kr) and I(Ks), which at present appear to be produced by the Kv HER gene and the KvLQT1 gene, respectively. Mutations of these two genes have been linked to two forms of hereditary long QT syndrome, and heterologous expression of mutant HERGs has reproduced the pathophysiological phenotype satisfactorily. Sporadic mutations in these and other cardiac K(+)channel genes may provide a basis for hypersensitivity to cardioactive or cardiotoxic drugs. (Trends Cardiovasc Med 1997;7:118-124). © 1997, Elsevier Science Inc.