Ionic mechanisms of the cardiac pacemaker potential.
The experimental evidence so far described in the literature is reviewed to explain the ionic mechanisms underlying the cardiac pacemaker potential in the sinoatrial node cell. Following gating mechanisms underlie the slow diastolic depolarization of the SA node cells. The delayed rectifier K+ channels (mainly the rapidly activated component of the delayed rectifier K+ currents, which is blocked by E-4031) activated during the preceding action potential are deactivated during diastole. The inactivation of the L-type Ca2+ channel is removed during the early diastolic period and results in an increasing inward current, provided that the amplitude of the window component is of significant amplitude. Because of its sustained nature, the removal of inactivation of the sustained inward current Ist, also generates inward current. The negative membrane potential near the maximum diastolic potential activates the hyperpolarization-activated non-selective cation current, I(f). Finally, the L-type Ca2+ channel is activated at the late phase of diastole depolarization, resulting in the maximum rate of rise of the action potential. These time- and voltage-dependent changes in membrane conductance occur in the presence of a significant background conductance. During the slow diastolic depolarization, Ist and IK may be the major component in the inward and outward currents, respectively.
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Department of Physiology, Faculty of Medicine, Kyoto University, Japan.
D000200:Action Potentials; D015220:Calcium Channels / Q000502:physiology; D003971:Diastole; D006801:Humans; D015640:Ion Channel Gating; D007474:Ion Exchange; D010138:Pacemaker, Artificial; D015221:Potassium Channels / Q000502:physiology; D012849:Sinoatrial Node / Q000166:cytology / Q000502:physiology*
D015220:Calcium Channels; D015221:Potassium Channels