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1 xpression is observed in the portions of the sinoatrial and atrioventricular junctions that are thoug
2 x30.2, which is most abundantly expressed in sinoatrial and atrioventricular nodal regions of the hea
5 .9 may slow propagation of excitation in the sinoatrial and atrioventricular nodes by shortening the
10 ntitative analysis and enables comparison of sinoatrial APs by standardizing parameter definitions an
12 pisodes of third-degree atrioventricular and sinoatrial block in every NaV1.5-immunized animal, but n
13 pe of unknown origin and atrioventricular or sinoatrial block lasting >10 seconds (average, 17.9+/-6.
14 tantial increases in atrial premature beats, sinoatrial block, and atrioventricular block, accompanie
16 a2 AMPK activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate
17 tric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholin
20 tation waves could enter the SAN through the sinoatrial conduction pathways and overdrive suppress th
21 Ch/Iso modulated filtering properties of the sinoatrial conduction pathways by increasing/decreasing
24 ged sinoatrial node recovery time, increased sinoatrial conduction time, and recurrent sinus pauses.
25 rial myocardium via superior and/or inferior sinoatrial exit pathways 8.8+/-3.2 mm from the leading p
27 for 2 (or more) narrow superior and inferior sinoatrial exit pathways separated by 12.8+/-4.1 mm.
30 pacemaker" current (I(f)) that increases the sinoatrial nodal (SAN) cell membrane diastolic depolariz
31 In wild-type mice, Ang II infusion caused sinoatrial nodal (SAN) cell oxidation by activating NADP
32 Dysregulation of L-type Ca(2+) currents in sinoatrial nodal (SAN) cells causes cardiac arrhythmia.
35 ted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model c
36 ulum (SR) during diastolic depolarization in sinoatrial nodal cells (SANC) occur even in the basal st
39 spontaneous diastolic depolarization (DD) of sinoatrial nodal cells (SANCs) that triggers recurrent a
41 s) increases the spontaneous beating rate of sinoatrial nodal cells (SANCs); however, the specific li
42 rs (RyRs) during diastolic depolarization of sinoatrial nodal cells augments the terminal depolarizat
44 raction) and the spontaneous beating rate of sinoatrial nodal cells were all blunted in RyR2-S2808A+/
47 uses, which were predominantly asymptomatic, sinoatrial nodal in origin, and nocturnal and occurred m
49 e of diastolic depolarization (DD) in rabbit sinoatrial nodal pacemaker cells (SANCs) generate an inw
51 lectively inhibits the funny current (If) in sinoatrial nodal tissue, resulting in a decrease in the
52 ine in situ detection of connexins in rabbit sinoatrial node (a tissue that is particularly rich in f
55 d indices of sympathovagal modulation of the sinoatrial node (ratio of low-frequency to high-frequenc
56 tructive heart surgery include injury of the sinoatrial node (SAN) and atrioventricular node (AVN), r
57 highly expressed in embryonic myocardium and sinoatrial node (SAN) and is required for cardiac automa
61 te the activation within the human or canine sinoatrial node (SAN) because they are intramural struct
62 rucial regulatory role in the development of sinoatrial node (SAN) by repressing the expression of Nk
65 t these sites and how this relates to normal sinoatrial node (SAN) development remain uncharacterized
67 polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of whi
68 primary pacemaker area of the intact rabbit sinoatrial node (SAN) exhibits robust positive labeling
69 d by Ras-related small G proteins, regulates sinoatrial node (SAN) ion channel activity through a mec
70 ght to confirm our hypothesis that the human sinoatrial node (SAN) is functionally insulated from the
72 her their presence nor their contribution to sinoatrial node (SAN) pacemaker activity has been invest
73 ated in controlling automaticity in isolated sinoatrial node (SAN) pacemaker cells, but the potential
75 rough K(+) channels are essential for proper sinoatrial node (SAN) pacemaking, but the influence of i
77 ces in cardiomyocyte automaticity permit the sinoatrial node (SAN) to function as the leading cardiac
78 Dysfunction of pacemaker activity in the sinoatrial node (SAN) underlies "sick sinus" syndrome (S
80 pecialized cardiomyocytes located within the sinoatrial node (SAN), and is responsible for originatin
84 situ studies indicated that Pitx2 suppresses sinoatrial node (SAN)-specific gene expression, includin
90 of this is the use of optical mapping in the sinoatrial node (SAN): when microelectrode and optical r
91 dly rectifying K+ (GIRK or KACh) channels of sinoatrial node and atria play a major role in beat-to-b
92 shown at birth to be present throughout the sinoatrial node and atrial muscle, however, at one month
94 ty of cell types and distribution within the sinoatrial node and cell-cell interactions add complexit
95 ntify Islet-1 as a novel marker of the adult sinoatrial node and do not provide evidence for Islet-1(
96 izes the leading pacemaker region within the sinoatrial node and hence is crucial for stable heart ra
97 the HCN1 protein is highly expressed in the sinoatrial node and is colocalized with HCN4, the main s
99 els of MiRP1 and HCN subunits in the cardiac sinoatrial node and the contribution of pacemaker channe
101 ) hearts the focus ultimately shifted to the sinoatrial node at a very prolonged cycle length (initia
102 t density contributes to the acceleration of sinoatrial node automaticity and explains, in part, the
106 r evaluated in rabbit isolated patch-clamped sinoatrial node cells (n = 21), where we found that 5 mu
108 neath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic
109 ct in concert with ion channels to confer on sinoatrial node cells (SANCs) their status of dominance
111 caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous
112 geneity of the electrical activity of single sinoatrial node cells as well as that of the intact sino
118 (as measured by cell capacitance) of rabbit sinoatrial node cells was investigated using the whole-c
119 n of pacemaker mechanisms in single isolated sinoatrial node cells, explanted beating sinoatrial node
124 ysis that Cx43 protein expression within the sinoatrial node decreased with age; however, the express
126 r conduction block and arrhythmias caused by sinoatrial node dysfunction are clinically important and
129 hmias: sinus pauses and bradycardia indicate sinoatrial node dysfunction, whereas preexcitation and a
131 P maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those obser
132 h-frequency ratio [P=0.03]) and less erratic sinoatrial node firing (eg, lower Poincare ratio [P=0.02
136 onic parasympathetic neurons innervating the sinoatrial node in control and HF dogs (both, n=8).
137 beta-adrenergic receptor stimulation of the sinoatrial node in intact dogs is markedly blunted when
141 ectrical signal is known to originate in the sinoatrial node myocyte, but exactly what role Ca plays
142 ow that depressed excitability of individual sinoatrial node myocytes (SAMs) contributes to reduction
145 ted sinoatrial node cells, explanted beating sinoatrial node preparation, telemetric in vivo electroc
146 nitiates early in development, represses the sinoatrial node program and pacemaker activity on the le
147 by bradycardia, sinus dysrhythmia, prolonged sinoatrial node recovery time, increased sinoatrial cond
148 We developed a computational model of the sinoatrial node that showed that a loss of SAN cells bel
151 pecifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting o
152 en by an electrical impulse generated in the sinoatrial node to propagate from atria to ventricles.
154 ional computerized numerical modeling of the sinoatrial node was conducted to validate the theoretica
157 within regions of the heart that become the sinoatrial node, atrioventricular node, and bundle of Hi
158 opagation of the action potential across the sinoatrial node, from the initiation point to the crista
159 [Ca(2+)]i release and Ca(2+) handling in the sinoatrial node, impaired pacemaker activity and symptom
162 ession and network analysis identified novel sinoatrial node-enriched genes and predicted that the tr
181 quency of pacemaker potentials from isolated sinoatrial pacemaker cells in the presence of endogenous
186 right vagosympathetic trunks innervated the sinoatrial plexus proximal to their entry into the heart
187 were contacted by fiber varicosities in the sinoatrial plexus than in the atrioventricular plexus af
192 e Ca(v)1.3 (alpha(1D)) Ca(2+) channel in the sinoatrial (SA) node by using Ca(v)1.3 Ca(2+) channel-de
194 on entry through L-type Ca2+ channels in the sinoatrial (SA) node contributes to pacemaker activity,
195 ontaneous activity of pacemaker cells in the sinoatrial (SA) node controls heart rate under normal ph
196 retation (mosaic model) of the makeup of the sinoatrial (SA) node has been proposed to explain the ch
197 on enzymatically isolated myocytes from the sinoatrial (SA) node, right and left atria, right and le
199 x5 expression is restricted to the posterior sinoatrial segments of the heart, consistent with the ti
200 ed at the venous pole in a plexus around the sinoatrial valve; mean total number of cells was 197 +/-
201 d channel 4, were located in the base of the sinoatrial valves, and this region was densely innervate
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