scholarly journals The Electrophysiological Properties of Spontaneously Beating Pacemaker Cells Isolated from Mouse Sinoatrial Node

2003 ◽  
Vol 550 (1) ◽  
pp. 169-180 ◽  
Author(s):  
Hyun‐Sung Cho ◽  
Makoto Takano ◽  
Akinori Noma
1999 ◽  
Vol 276 (4) ◽  
pp. H1295-H1304 ◽  
Author(s):  
Haruo Honjo ◽  
Ming Lei ◽  
Mark R. Boyett ◽  
Itsuo Kodama

The electrophysiological properties of sinoatrial (SA) node pacemaker cells vary in different regions of the node. In this study, we have investigated variation of the 4-aminopyridine (4-AP)-sensitive current as a function of the size (as measured by the cell capacitance) of SA node cells to elucidate the ionic mechanisms. The 10 mM 4-AP-sensitive current recorded from rabbit SA node cells was composed of transient and sustained components ( I trans and I sus, respectively). The activation and inactivation properties [activation: membrane potential at which conductance is half-maximally activated ( V h) = 19.3 mV, slope factor ( k) = 15.0 mV; inactivation: V h= −31.5 mV, k = 7.2 mV] as well as the density of I trans (9.0 pA/pF on average at +50 mV) were independent of cell capacitance. In contrast, the density of I sus (0.97 pA/pF on average at +50 mV) was greater in larger cells, giving rise to a significant correlation with cell capacitance. The greater density of I sus in larger cells (presumably from the periphery) can explain the shorter action potential in the periphery of the SA node compared with that in the center. Thus variation of the 4-AP-sensitive current may be involved in regional differences in repolarization within the SA node.


1986 ◽  
Vol 250 (3) ◽  
pp. H397-H406 ◽  
Author(s):  
G. J. Rozanski ◽  
J. Jalife

Microelectrode techniques were used to study the electrophysiological properties of pacemaker fibers in isolated atrioventricular valves of the rabbit heart. In spontaneously beating tricuspid and mitral valve preparations superfused with normal Tyrode solution, leading pacemaker activity was generated by fibers located on the valve leaflet. Impulse conduction from the automatic focus to atrial myocardium was slow, and in approximately 50% of preparations, exit block occurred. Valve pacemaker fibers had significantly different action potential characteristics compared with the primary pacemaker cells of the sinoatrial node. However, the activity of both pacemaker types was largely insensitive to tetrodotoxin but readily suppressed by verapamil. Endogenous neurotransmitters, released from postganglionic nerve endings in the vicinity of valve pacemaker fibers, exerted profound chrono- and dromotropic effects. Brief cholinergic stimuli strongly influenced valve pacemaker cycle length in a phase-dependent manner, qualitatively similar to that in the sinoatrial node. During overdrive of valve pacemaker fibers with external bipolar stimuli, locally released neurotransmitters modified automaticity and conduction which, under certain conditions, favored pacemaker escape. These data demonstrate that the atrioventricular valve leaflets contain cardiac fibers capable of generating spontaneous impulses and that intrinsic autonomic nerves may play a role in precipitating premature extrasystoles.


2012 ◽  
Vol 302 (9) ◽  
pp. H1773-H1783 ◽  
Author(s):  
Vadim V. Fedorov ◽  
Alexey V. Glukhov ◽  
Roger Chang

Since Keith and Flack's anatomical discovery of the sinoatrial node (SAN), the primary pacemaker of the heart, the question of how such a small SAN structure can pace the entire heart has remained for a large part unanswered. Recent advances in optical mapping technology have made it possible to unambiguously resolve the origin of excitation and conduction within the animal and human SAN. The combination of high-resolution optical mapping and histological structural analysis reveals that the canine and human SANs are functionally insulated from the surrounding atrial myocardium, except for several critical conduction pathways. Indeed, the SAN as a leading pacemaker requires anatomical (fibrosis, fat, and blood vessels) and/or functional barriers (paucity of connexins) to protect it from the hyperpolarizing influence of the surrounding atrium. The presence of conduction barriers and pathways may help explain how a small cluster of pacemaker cells in the SAN pacemaker complex manages to depolarize different, widely distributed areas of the right atria as evidenced functionally by exit points and breakthroughs. The autonomic nervous system and humoral factors can further regulate conduction through these pathways, affecting pacemaker automaticity and ultimately heart rate. Moreover, the conduction barriers and multiple pathways can form substrates for reentrant activity and thus lead to atrial flutter and fibrillation. This review aims to provide new insight into the function of the SAN pacemaker complex and the interaction between the atrial pacemakers and the surrounding atrial myocardium not only in animal models but also human hearts.


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