Abstract
Intracellular Ca2+-mediated mechanisms for pacemaker depolarization were studied in sinus node tissue preparations from mice and guinea pigs. Microelectrode recordings revealed that the sinus node of the mouse, which had a higher beating rate, had a steeper slope of the pacemaker depolarization than that of the guinea pig. BAPTA and ryanodine, agents that interfere with intracellular Ca2+, significantly decreased the slope of the pacemaker depolarization in both species. In contrast, SEA0400, a specific inhibitor of the Na+-Ca2+ exchanger (NCX), as well as change to low Na+ extracellular solution, significantly decreased the slope in the mouse, but not in the guinea pig. Niflumic acid, a blocker of the Ca2+ activated Cl− channel, decreased the slope in both species. Confocal microscopy revealed the presence of spontaneous Ca2+ oscillations during the interval between Ca2+ transients; such phenomenon was more pronounced in the mouse than in the guinea pig. Thus, although intracellular Ca2+-mediated mechanisms were involved in the pacemaker depolarization of the sinus node in both species, the NCX current was involved in the mouse but not in the guinea pig.
Highlights
The contraction of the myocardium is driven by the action potential originating in the sinus node, the cardiac pacemaker
The sinus node consists of cardiomyocytes with different electrophysiological properties [5,11], and these cells work as a functional syncytium to form the pacemaker depolarization
Microelectrode recordings showed that the sinus node of the mouse, which had a higher firing rate, had a steeper slope of the pacemaker depolarization and a shorter action potential duration than that of the guinea pig
Summary
The contraction of the myocardium is driven by the action potential originating in the sinus node, the cardiac pacemaker. The combination of membrane currents involved in the pacemaker depolarization appears to be different among animal species. Exchanger (NCX) to generate a depolarizing current and accelerate the pacemaker depolarization This mechanism was referred to as the Ca2+ clock and was considered to function in coordination with the ion channels of the cell membrane (membrane clock) to form the pacemaker depolarization [8,9]. The related experimental results appear to vary among researchers, and definitive conclusions have not been reached for the involvement of intracellular Ca2+ -mediated mechanisms or the precise pacemaking mechanisms in each animal species. The sinus node consists of cardiomyocytes with different electrophysiological properties [5,11], and these cells work as a functional syncytium to form the pacemaker depolarization. We intended to clarify the involvement of intracellular Ca2+ -mediated mechanisms in the pacemaker depolarization of the mouse and guinea pig sinus node using tissue preparations. We performed standard microelectrode measurements of action potentials with sinus node tissue preparations and applied selective pharmacological agents
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