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1 adycardia, consistent with AC9 expression in sinoatrial node.
2 nscriptional regulator within the developing sinoatrial node.
3 otein was not expressed in the centre of the sinoatrial node.
4 lowering agent that acts specifically on the sinoatrial node.
5  of ionic currents in pacemaker cells of the sinoatrial node.
6 ial node cells as well as that of the intact sinoatrial node.
7       It also is present in areas within the sinoatrial node.
8 properties of pacemaker myocytes in the aged sinoatrial node.
9 sistently Islet-1 mRNA was detected in human sinoatrial node.
10 unction, with initial, larger effects on the sinoatrial node.
11 er-law behavior comparable to those of human sinoatrial node.
12 The AVJ is a primary backup pacemaker to the sinoatrial node.
13  may mask intrinsic fractal behaviour of the sinoatrial node.
14 and peripheral cells that make up the native sinoatrial node.
15 right atrial foci, especially those near the sinoatrial node.
16 e wall, corresponding to the location of the sinoatrial node.
17 ine in situ detection of connexins in rabbit sinoatrial node (a tissue that is particularly rich in f
18 dly rectifying K+ (GIRK or KACh) channels of sinoatrial node and atria play a major role in beat-to-b
19  shown at birth to be present throughout the sinoatrial node and atrial muscle, however, at one month
20 ls is required for proper hearing as well as sinoatrial node and brain function.
21 ty of cell types and distribution within the sinoatrial node and cell-cell interactions add complexit
22 ntify Islet-1 as a novel marker of the adult sinoatrial node and do not provide evidence for Islet-1(
23 izes the leading pacemaker region within the sinoatrial node and hence is crucial for stable heart ra
24  the HCN1 protein is highly expressed in the sinoatrial node and is colocalized with HCN4, the main s
25 ardiac myocytes and specialized cells in the sinoatrial node and the conduction system.
26 els of MiRP1 and HCN subunits in the cardiac sinoatrial node and the contribution of pacemaker channe
27                                          The sinoatrial node and the ventricle of the heart receive s
28           Given that other biological (e.g., sinoatrial node) and artificial systems display phase-lo
29 ) hearts the focus ultimately shifted to the sinoatrial node at a very prolonged cycle length (initia
30 in isolated guinea pig spontaneously beating sinoatrial node/atrial preparations.
31  within regions of the heart that become the sinoatrial node, atrioventricular node, and bundle of Hi
32 t density contributes to the acceleration of sinoatrial node automaticity and explains, in part, the
33                                              Sinoatrial node automaticity was slowed in treated group
34  recorded from isolated papillary muscle and sinoatrial node by microelectrode techniques.
35  current appearing in the Noble model of the sinoatrial node cell in the mammalian heart.
36 r evaluated in rabbit isolated patch-clamped sinoatrial node cells (n = 21), where we found that 5 mu
37                Spontaneous beating of rabbit sinoatrial node cells (SANCs) is controlled by cAMP-medi
38 neath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic
39 ct in concert with ion channels to confer on sinoatrial node cells (SANCs) their status of dominance
40  roughly periodic LCRs in depolarized rabbit sinoatrial node cells (SANCs).
41  caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous
42 geneity of the electrical activity of single sinoatrial node cells as well as that of the intact sino
43             Spontaneous action potentials of sinoatrial node cells from pregnant mice exhibited highe
44                   The electrical activity of sinoatrial node cells is heterogeneous.
45  intracellular cAMP levels were unchanged in sinoatrial node cells of pregnant mice.
46                                           In sinoatrial node cells of the heart, beating rate is cont
47 ted inward current similar to the If seen in sinoatrial node cells of the heart.
48  (as measured by cell capacitance) of rabbit sinoatrial node cells was investigated using the whole-c
49 n of pacemaker mechanisms in single isolated sinoatrial node cells, explanted beating sinoatrial node
50 ergically stimulated ion channels in cardiac sinoatrial node cells.
51 .0 pA/pF; P, -28.6+/-2.9 pA/pF; P=0.0002) in sinoatrial node cells.
52 the slope of the diastolic depolarization of sinoatrial node cells.
53 on of spontaneous action potential firing in sinoatrial node cells.
54 ysis that Cx43 protein expression within the sinoatrial node decreased with age; however, the express
55 uch as Shox2 and Tbx3, that are required for sinoatrial node development.
56 r conduction block and arrhythmias caused by sinoatrial node dysfunction are clinically important and
57                                              Sinoatrial node dysfunction associated with CPVT may inc
58             Clinical studies have shown that sinoatrial node dysfunction occurs at the highest incide
59 hmias: sinus pauses and bradycardia indicate sinoatrial node dysfunction, whereas preexcitation and a
60 ation and miR-106b-25 heterozygosity develop sinoatrial node dysfunction.
61 ession and network analysis identified novel sinoatrial node-enriched genes and predicted that the tr
62 P maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those obser
63 h-frequency ratio [P=0.03]) and less erratic sinoatrial node firing (eg, lower Poincare ratio [P=0.02
64 opagation of the action potential across the sinoatrial node, from the initiation point to the crista
65               The age-dependent reduction in sinoatrial node function was not associated with changes
66  vagal activity, baroreceptor responses, and sinoatrial node function.
67 x2 regulates microRNAs (miRs) to repress the sinoatrial node genetic program.
68 ted in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4).
69 [Ca(2+)]i release and Ca(2+) handling in the sinoatrial node, impaired pacemaker activity and symptom
70 onic parasympathetic neurons innervating the sinoatrial node in control and HF dogs (both, n=8).
71  beta-adrenergic receptor stimulation of the sinoatrial node in intact dogs is markedly blunted when
72 h incidence of bradycardia suggests possible sinoatrial node involvement.
73 y definition, that pacemaker function of the sinoatrial node is compromised during aging.
74                                          The sinoatrial node is the main impulse-generating tissue in
75 ectrical signal is known to originate in the sinoatrial node myocyte, but exactly what role Ca plays
76 ow that depressed excitability of individual sinoatrial node myocytes (SAMs) contributes to reduction
77                                              Sinoatrial node myocytes act as cardiac pacemaker cells
78 canine AVJ preparations that did not contain sinoatrial node (n = 10).
79 +) cells in the right atrium coexpressed the sinoatrial node pacemaker cell marker HCN4.
80 ted sinoatrial node cells, explanted beating sinoatrial node preparation, telemetric in vivo electroc
81 nitiates early in development, represses the sinoatrial node program and pacemaker activity on the le
82 d indices of sympathovagal modulation of the sinoatrial node (ratio of low-frequency to high-frequenc
83 by bradycardia, sinus dysrhythmia, prolonged sinoatrial node recovery time, increased sinoatrial cond
84 tructive heart surgery include injury of the sinoatrial node (SAN) and atrioventricular node (AVN), r
85 highly expressed in embryonic myocardium and sinoatrial node (SAN) and is required for cardiac automa
86                Experiments were performed on sinoatrial node (SAN) and latent atrial pacemaker (LAP)
87               Numerous studies implicate the sinoatrial node (SAN) as a participant in atrial arrhyth
88 ane voltage and Ca2+ clocks jointly regulate sinoatrial node (SAN) automaticity.
89 te the activation within the human or canine sinoatrial node (SAN) because they are intramural struct
90 rucial regulatory role in the development of sinoatrial node (SAN) by repressing the expression of Nk
91 olecular and functional properties of native sinoatrial node (SAN) cardiomyocytes.
92                                           In sinoatrial node (SAN) cells, electrogenic sodium-calcium
93 t these sites and how this relates to normal sinoatrial node (SAN) development remain uncharacterized
94                                     Although sinoatrial node (SAN) dysfunction is a hallmark of human
95 polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of whi
96  primary pacemaker area of the intact rabbit sinoatrial node (SAN) exhibits robust positive labeling
97 d by Ras-related small G proteins, regulates sinoatrial node (SAN) ion channel activity through a mec
98 ght to confirm our hypothesis that the human sinoatrial node (SAN) is functionally insulated from the
99                                          The sinoatrial node (SAN) maintains a rhythmic heartbeat; th
100 her their presence nor their contribution to sinoatrial node (SAN) pacemaker activity has been invest
101 ated in controlling automaticity in isolated sinoatrial node (SAN) pacemaker cells, but the potential
102  in embryonic heart, but their role in adult sinoatrial node (SAN) pacemaking is uncertain.
103 rough K(+) channels are essential for proper sinoatrial node (SAN) pacemaking, but the influence of i
104 ated current, If, plays an important role in sinoatrial node (SAN) pacemaking.
105 ces in cardiomyocyte automaticity permit the sinoatrial node (SAN) to function as the leading cardiac
106     Dysfunction of pacemaker activity in the sinoatrial node (SAN) underlies "sick sinus" syndrome (S
107          The heartbeat originates within the sinoatrial node (SAN), a small structure containing <10,
108 pecialized cardiomyocytes located within the sinoatrial node (SAN), and is responsible for originatin
109                                          The sinoatrial node (SAN), functionally known as the pacemak
110          Reentrant arrhythmias involving the sinoatrial node (SAN), namely SAN reentry, remain one of
111 ify ion channel transcripts expressed in the sinoatrial node (SAN), the pacemaker of the heart.
112 situ studies indicated that Pitx2 suppresses sinoatrial node (SAN)-specific gene expression, includin
113 R) modulates the spontaneous activity of the sinoatrial node (SAN).
114 te (HR) by inhibiting pacemaker cells in the sinoatrial node (SAN).
115 bx18 give rise to the heart's pacemaker, the sinoatrial node (SAN).
116 by specialized cardiomyocytes located in the sinoatrial node (SAN).
117 ia and ventricles, there is no model for the sinoatrial node (SAN).
118 of this is the use of optical mapping in the sinoatrial node (SAN): when microelectrode and optical r
119    We developed a computational model of the sinoatrial node that showed that a loss of SAN cells bel
120                        During failure of the sinoatrial node, the heart can be driven by an atriovent
121                                  Passing the sinoatrial node, the P-wave developed an initial positiv
122 coupling was investigated by dye transfer in sinoatrial node tissue explants.
123                            RNA sequencing on sinoatrial node tissue lacking Islet-1 established that
124 pecifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting o
125 en by an electrical impulse generated in the sinoatrial node to propagate from atria to ventricles.
126 uction system, extending proximally from the sinoatrial node to the distal Purkinje fibers.
127 ional computerized numerical modeling of the sinoatrial node was conducted to validate the theoretica
128 s is controversial despite the fact that the sinoatrial node was discovered over 100 years ago.

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