Cardiac action potential (AP) initiatesand coordinates the contraction of the heart through the co-operation inopening and closing of voltage- and ligand-gated ion channels of myocyte SL(Bers, 2001).
Ion current densities and channel compositions reveal regionalspecialization in the heart, i.e. each cardiac chamber has distinct andfunctionally AP. Pacemaker APs, initiatethe spontaneous beating of the heart, are characterized by a slowdepolarization of membrane potential during diastole. Contrary, atrial andventricular APs have a clearly stable resting membrane potential (RMP) about-80 mV with a fast depolarization. There is a striking difference betweenatrial and ventricular AP duration, where atrial AP duration is shorter thanthe ventricular AP (Saito and Tenma, 1976; Haverinen and Vornanen, 2009; Lin etal., 2014; Vornanen, 2016). Changes in membrane voltage assosiated with the AP requireelectrical charges to be transferred through the specific ion channels ofmyosyte SL which mainly controled by Na+, Ca2+ and K+ions.
As otherverteprates, fish cardiac AP can be divided into 5 phases (0-4) (Fozzard, 1977;Roden et al., 2002; Vornanen, 2016). A resting cardiomyocyte has a stableresting membrane potential (RMP) of -70 to -90 mV in atrial and ventricularmyocytes relative to the extracellular fluid (phase 4) which maintained by a effluxof K+ ions through specific SL potassium channels. The resting casebroken by a voltage spread from neighboring myocytes (depolarization) and excitethe resting myocyte for contraction. After depolarization, RMP moves towardpositive voltages (threshold potential; TP), where the density of the inward Na+current exceeds the total density of the outward K+ currents, a fastupstroke of the AP is generated and within a few ms the membrane is shiftedfrom the threshold potential to a voltage above the zero level (phase 0). Phase0 is produced by Na+ influx into the myocyte through SL Na channels.
the density of Na+ current is the major factor in determining therate of AP propagation over atrial and ventricular myocytes, i.e., the largerNa+ influx causes the fatser AP upstroke. AP upstroke is followed byrapid reploarization (phase 1) which generated by the transient outward K+current. In contrast with mammalian cardiac APs, phase 1 is often inconspeciousor absent in fish cardiac myocytes. Thelongest stage of AP (phase 2) is called “plateau phase” where the balancebetween inward Ca2+ current and outward K+ currentoccurred.
Phase 2 is essential for Ca2+ influx and cardiaccontraction, and preventsthe heart from beating prematurely by delaying the recovery of Na+channels from inactivated state. The fast restoration of the negativeRMP starts at the end of the plateau phase (phase 3), which produced by variousoutward K+ currents (delayed rectifier K+ current, inwardrectifier K+ current and slow component of delayed rectifier K+current). Restoration of RMP is crucial for the heart in diastole phase andallows blood to fill the atrium and ventricle. Finally thecomplete restoration of the negative RMP (phase 4).Atrial andventricular APs have the same 5 phases of cardiac AP in the fish heart.
However, there is a significant difference between atrial and ventricularmyocytes in AP duration, where atrial AP is much shorter than ventricular AP(Saito and Tenma, 1976; Haverinen and Vornanen, 2009; Lin et al., 2014). Incontrast to the stable RMP of atrial and ventricular myocytes, pacemaker APsare characterized by gradual and slow diastolic depolarization towards thethreshold voltage of the AP upstroke (Saito, 1969; Saito, 1973; Harper et al.,1995; Haverinen and Vornanen, 2007; Tessadori et al.
, 2012). Amplitude andduration of the pacemaker AP is smaller and the rate of upstroke andrepolarization slower than those of atrial and ventricular APs. Transmission ofpacemaker APs to the neighboring atrial myocytes depolarizes them and startsthe spread of electrical excitation throughout the heart.
