Potassium channels in cardiac cells

摘要

K+channels in heart can be subdivided into two groups, voltage-operated and ligand-operated channels. Only the voltage-operated channels—iK, ito, and iK1—and one ligand-operated channel—iK(ACh)—are activated under physiological conditions; the iK1only carries large currents at the resting potential. The delayed K+current, iK, and the transient outward current, ito, are important for the plateau and repolarization phase of the action potential, and thus affect the refractory period in atrial and ventricular cells and also the frequency in the sinoatrial node. A high density of itoand iCais responsible for the spike-dome appearance of the plateau phase in adult atrial cells, epicardial myocytes, and Purkinje cells stimulated by catecholamines. The action-potential duration in these cells is more sensitive to Ke+, frequency, and drugs. The iK(ACh)can also be activated by adenosine and somatostatin. Its density is high in nodal and atrial tissue. Under pathological conditions, K+channels dependent on ATP, Nai+, and fatty acids are activated and can carry large currents at depolarized levels. Local changes in the concentration of ATP or Na close to the membrane are probably important for the activation process. The study of pharmacological modulation of K+currents should include frequency effects for the voltage-activated c