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The cardiac action potential is a short-lasting event in which the membrane potential (the difference of potential between the interior and the exterior) of a cardiac cell rises and falls following a consistent trajectory, similar to the action potential in other types of cells. The cardiac action potential differs significantly in different portions of the heart. The heart is provided with a special excitatory system and a contractile system necessary to differentiate action potentials in the heart, which allow it to function at a constant rate. This differentiation of the action potentials allows the different electrical characteristics of the different portions of the heart. For instance, the specialized excitatory system of the heart has the special property of spontaneous depolarization. This means the heart depolarizes without any external influence via a slow, positive increase in voltage known as the pacemaker potential across the cell's membrane (the membrane potential) that occurs between the end of one action potential and the beginning of the next action potential. This increase in membrane potential (depolarization) typically allows it to reach the threshold potential at which the next pacemaker potential is fired. Thus, it is the pacemaker potential that drives the self-generated rhythmic firing, known as cardiac muscle automaticity or autorhythmicity. Pacemaker potentials are fired by sinoatrial node (SAN), but also by the other foci. However, the last ones have firing frequencies slower than the SAN's. When other foci attempt to fire at their intrinsic rate, they can not, because they have been discharged by the previous electric impulse coming from the SAN before their pacemaker potential threshold is reached. This is called "overdrive suppression". Under certain conditions (if pacemaker cells become compromised) non-pacemaker cells can take over and set the pace of the heart (become pacemakers). Rate dependence of action potential is a fundamental property of cardiac cells. This is important for the QT interval, measured from the beginning of the QRS complex to the end of the T wave. This interval must be corrected for the cardiac rhythm QTc. A prolonged QTc, long QT syndrome, induced by drugs or disease congenital or acquired, increases the possibility of developing severe ventricular arrhythmias and sometimes sudden death. The electrical activity of the specialized excitatory tissues is not apparent on the surface electrocardiogram (ECG). This is due to the relatively small time duration. It is not possible, for example, to see on the ECG the sinus node activity, but the resulting atrial myocardium contraction is apparent as a wave – the P wave. The electrical activity of the conducting system can be seen on the ECG (for example the AV node delay and the so-called PR segment). ==Overview== Cardiac action potentials are generated by the movement of ions through the transmembrane ion channels in the cardiac cells. Cardiac muscle bears some similarities to skeletal muscle, as well as important differences. Like skeletal myocytes (and axons for that matter), in the resting state a given cardiac myocyte has a negative membrane potential. Within the cell K+(potassium) is the principal cation, and phosphate and the conjugate bases of organic acids are the dominant anions. Outside the cell Na+ (sodium) is the principal cation and Cl− (chloride) is the dominant anion. A notable difference between skeletal and cardiac myocytes is how each elevates the myoplasmic Ca2+ to induce contraction. When skeletal muscle is stimulated by somatic motor axons, influx of Na+ quickly depolarizes the skeletal myocyte and triggers calcium release from the sarcoplasmic reticulum. However, in cardiac myocytes the release of Ca2+ from the sarcoplasmic reticulum is induced by Ca2+ influx into the cell through voltage-gated calcium channels on the sarcolemma. This phenomenon is called calcium-induced calcium release and increases the myoplasmic free Ca2+ concentration causing muscle contraction. In both muscle types, after a delay (the absolute refractory period), potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization. The voltage-gated calcium channels in the cardiac sarcolemma are generally triggered by an influx in sodium during the "0" phase of the action potential (see below). Cardiac muscle is a syncytium in which the cardiac muscle cells are so tightly bound that when one of these cells is excited the action potential spreads to all of them and allows succinct coordinated contraction of the heart. Cardiac pacemaker cells (autorhythmic cells) are connected to adjoining contractile cells (non-pacemaker cells) via gap junctions. Gap junctions allow the spontaneous depolarization and action potential generated by pacemaker cells to be transferred to contractile cells. Of all the cells in the body, only heart cells are able to contract on their own without stimulation from the nervous system. There are important physiological differences between excitatory cells and muscular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of excitatory cells, most importantly the spontaneous depolarization (cardiac muscle automaticity) necessary for the SAN pacemaker activity. Atrial myocytes, ventricular myocytes and Purkinje cells are examples of non-pacemaker action potentials in the heart. Because these action potentials undergo very rapid depolarization, they are sometimes referred to as "fast response" action potentials 〔Klabunde, Richard. "Non-pacemaker Action Potentials". Richard E. Klabund, 2008. ().〕 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Cardiac action potential」の詳細全文を読む スポンサード リンク
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