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1 and peripheral cells that make up the native sinoatrial node.
2 right atrial foci, especially those near the sinoatrial node.
3 e wall, corresponding to the location of the sinoatrial node.
4 e ganglia, respectively, that project to the sinoatrial node.
5 otein was not expressed in the centre of the sinoatrial node.
6 lowering agent that acts specifically on the sinoatrial node.
7  of ionic currents in pacemaker cells of the sinoatrial node.
8 ial node cells as well as that of the intact sinoatrial node.
9       It also is present in areas within the sinoatrial node.
10 aneous firing rate of pacemaker cells in the sinoatrial node.
11 role in generating pacemaker activity of the sinoatrial node.
12 s from RIalpha-icKO mice but not in atria or sinoatrial node.
13 adycardia, consistent with AC9 expression in sinoatrial node.
14  discovered nonfiring pacemaker cells in the sinoatrial node.
15 wave of electrical activity initiated at the sinoatrial node.
16 unction, with initial, larger effects on the sinoatrial node.
17 nscriptional regulator within the developing sinoatrial node.
18 properties of pacemaker myocytes in the aged sinoatrial node.
19 sistently Islet-1 mRNA was detected in human sinoatrial node.
20 er-law behavior comparable to those of human sinoatrial node.
21 CN4 for the central pacemaker process in the sinoatrial node.
22 The AVJ is a primary backup pacemaker to the sinoatrial node.
23  may mask intrinsic fractal behaviour of the sinoatrial node.
24 ine in situ detection of connexins in rabbit sinoatrial node (a tissue that is particularly rich in f
25 dly rectifying K+ (GIRK or KACh) channels of sinoatrial node and atria play a major role in beat-to-b
26  shown at birth to be present throughout the sinoatrial node and atrial muscle, however, at one month
27 ls is required for proper hearing as well as sinoatrial node and brain function.
28 ty of cell types and distribution within the sinoatrial node and cell-cell interactions add complexit
29 ntify Islet-1 as a novel marker of the adult sinoatrial node and do not provide evidence for Islet-1(
30 izes the leading pacemaker region within the sinoatrial node and hence is crucial for stable heart ra
31  the HCN1 protein is highly expressed in the sinoatrial node and is colocalized with HCN4, the main s
32 ardiac myocytes and specialized cells in the sinoatrial node and the conduction system.
33 els of MiRP1 and HCN subunits in the cardiac sinoatrial node and the contribution of pacemaker channe
34                                          The sinoatrial node and the ventricle of the heart receive s
35 ocal gene expression to resemble that of the sinoatrial node and unleashed automaticity originating a
36           Given that other biological (e.g., sinoatrial node) and artificial systems display phase-lo
37   We found that cardiomyocytes of the atria, sinoatrial node, and ventricular conduction system expre
38     Pacemaker cardiomyocytes that create the sinoatrial node are essential for the initiation and mai
39 ) hearts the focus ultimately shifted to the sinoatrial node at a very prolonged cycle length (initia
40 in isolated guinea pig spontaneously beating sinoatrial node/atrial preparations.
41  within regions of the heart that become the sinoatrial node, atrioventricular node, and bundle of Hi
42 ugh the components of the CCS, including the sinoatrial node, atrioventricular node, His bundle, bund
43       Here, we review the latest findings on sinoatrial node automaticity and discuss the physiologic
44 t density contributes to the acceleration of sinoatrial node automaticity and explains, in part, the
45                                              Sinoatrial node automaticity was slowed in treated group
46  recorded from isolated papillary muscle and sinoatrial node by microelectrode techniques.
47  current appearing in the Noble model of the sinoatrial node cell in the mammalian heart.
48 r evaluated in rabbit isolated patch-clamped sinoatrial node cells (n = 21), where we found that 5 mu
49                Spontaneous beating of rabbit sinoatrial node cells (SANCs) is controlled by cAMP-medi
50 neath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic
51 ct in concert with ion channels to confer on sinoatrial node cells (SANCs) their status of dominance
52  roughly periodic LCRs in depolarized rabbit sinoatrial node cells (SANCs).
53  caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous
54 geneity of the electrical activity of single sinoatrial node cells as well as that of the intact sino
55 m cell differentiation cultures enriches for sinoatrial node cells exhibiting a functional pacemaker
56             Spontaneous action potentials of sinoatrial node cells from pregnant mice exhibited highe
57 and the targeted delivery of therapeutics to sinoatrial node cells in vivo using antibody-drug conjug
58                   The electrical activity of sinoatrial node cells is heterogeneous.
59  intracellular cAMP levels were unchanged in sinoatrial node cells of pregnant mice.
60                                           In sinoatrial node cells of the heart, beating rate is cont
61 ted inward current similar to the If seen in sinoatrial node cells of the heart.
62 etal and human pluripotent stem cell-derived sinoatrial node cells to reveal that they consist of thr
63  (as measured by cell capacitance) of rabbit sinoatrial node cells was investigated using the whole-c
64 n of pacemaker mechanisms in single isolated sinoatrial node cells, explanted beating sinoatrial node
65 ergically stimulated ion channels in cardiac sinoatrial node cells.
66 tes to the pacemaker current (I(f)) in human sinoatrial node cells.
67 .0 pA/pF; P, -28.6+/-2.9 pA/pF; P=0.0002) in sinoatrial node cells.
68 the slope of the diastolic depolarization of sinoatrial node cells.
69 on of spontaneous action potential firing in sinoatrial node cells.
70 ysis that Cx43 protein expression within the sinoatrial node decreased with age; however, the express
71 uch as Shox2 and Tbx3, that are required for sinoatrial node development.
72 r conduction block and arrhythmias caused by sinoatrial node dysfunction are clinically important and
73                                              Sinoatrial node dysfunction associated with CPVT may inc
74             Clinical studies have shown that sinoatrial node dysfunction occurs at the highest incide
75 d cation channels may protect the heart from sinoatrial node dysfunction, secondary arrhythmia of the
76 hmias: sinus pauses and bradycardia indicate sinoatrial node dysfunction, whereas preexcitation and a
77 ation and miR-106b-25 heterozygosity develop sinoatrial node dysfunction.
78 ite dysregulation of PITX2 expression in the sinoatrial node (ectopic activation) and ventricle (redu
79 ession and network analysis identified novel sinoatrial node-enriched genes and predicted that the tr
80 mechanisms; underlies time-of-day changes in sinoatrial node excitability/intrinsic heart rate; and l
81 P maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those obser
82 h-frequency ratio [P=0.03]) and less erratic sinoatrial node firing (eg, lower Poincare ratio [P=0.02
83 opagation of the action potential across the sinoatrial node, from the initiation point to the crista
84               The age-dependent reduction in sinoatrial node function was not associated with changes
85  of conduction abnormalities and compromised sinoatrial node function which could lead to increased r
86  vagal activity, baroreceptor responses, and sinoatrial node function.
87 x2 regulates microRNAs (miRs) to repress the sinoatrial node genetic program.
88 ted in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4).
89 [Ca(2+)]i release and Ca(2+) handling in the sinoatrial node, impaired pacemaker activity and symptom
90 onic parasympathetic neurons innervating the sinoatrial node in control and HF dogs (both, n=8).
91  beta-adrenergic receptor stimulation of the sinoatrial node in intact dogs is markedly blunted when
92 h incidence of bradycardia suggests possible sinoatrial node involvement.
93                             We show that the sinoatrial node is compartmentalized, with a core of pac
94 y definition, that pacemaker function of the sinoatrial node is compromised during aging.
95 lular and molecular composition of the human sinoatrial node is not resolved.
96                                          The sinoatrial node is the main impulse-generating tissue in
97 In this study, we have assessed the roles of sinoatrial node L-type Ca(v)1.3 (alpha(1D)) Ca(2+) chann
98 ectrical signal is known to originate in the sinoatrial node myocyte, but exactly what role Ca plays
99                                              Sinoatrial node myocytes (SAMs) act as cardiac pacemaker
100 ow that depressed excitability of individual sinoatrial node myocytes (SAMs) contributes to reduction
101                                              Sinoatrial node myocytes act as cardiac pacemaker cells
102 canine AVJ preparations that did not contain sinoatrial node (n = 10).
103 g of the intrinsic pacemaker activity of the sinoatrial node of the heart, which results from electri
104 ctive blocker of the I(funny) channel in the sinoatrial node) on heart rate, quality of life (QOL), a
105 +) cells in the right atrium coexpressed the sinoatrial node pacemaker cell marker HCN4.
106                                         This sinoatrial node pacemaker cell surface marker is highly
107  cell surface marker to identify and isolate sinoatrial node pacemaker cells has been reported.
108               Our study identifies a host of sinoatrial node pacemaker markers including MYH11, BMP4,
109                         In an ex vivo murine sinoatrial node preparation, addition of the K(Ca)1.1 an
110 ted sinoatrial node cells, explanted beating sinoatrial node preparation, telemetric in vivo electroc
111 nitiates early in development, represses the sinoatrial node program and pacemaker activity on the le
112 d indices of sympathovagal modulation of the sinoatrial node (ratio of low-frequency to high-frequenc
113 by bradycardia, sinus dysrhythmia, prolonged sinoatrial node recovery time, increased sinoatrial cond
114 the greatest density of innervation near the sinoatrial node region (P < 0.05, n = 6).
115 odissection were isolated, including: Zone I-sinoatrial node region; Zone II-atrioventricular node/Hi
116                                          The sinoatrial node regulates the heart rate throughout life
117  of the human cardiac conduction system: the sinoatrial node (SAN) and atrioventricular node (AVN), r
118 tructive heart surgery include injury of the sinoatrial node (SAN) and atrioventricular node (AVN), r
119 highly expressed in embryonic myocardium and sinoatrial node (SAN) and is required for cardiac automa
120                Experiments were performed on sinoatrial node (SAN) and latent atrial pacemaker (LAP)
121               Numerous studies implicate the sinoatrial node (SAN) as a participant in atrial arrhyth
122 ane voltage and Ca2+ clocks jointly regulate sinoatrial node (SAN) automaticity.
123 te the activation within the human or canine sinoatrial node (SAN) because they are intramural struct
124 rucial regulatory role in the development of sinoatrial node (SAN) by repressing the expression of Nk
125 olecular and functional properties of native sinoatrial node (SAN) cardiomyocytes.
126 m (ANS) and intrinsic mechanisms that govern sinoatrial node (SAN) cell function.
127                                           In sinoatrial node (SAN) cells, electrogenic sodium-calcium
128 t these sites and how this relates to normal sinoatrial node (SAN) development remain uncharacterized
129                         Mechanisms for human sinoatrial node (SAN) dysfunction are poorly understood
130                                     Although sinoatrial node (SAN) dysfunction is a hallmark of human
131                                              Sinoatrial node (SAN) dysfunction is commonly associated
132 polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of whi
133 lure (HF) is frequently accompanied with the sinoatrial node (SAN) dysfunction, which causes tachy-br
134  primary pacemaker area of the intact rabbit sinoatrial node (SAN) exhibits robust positive labeling
135 ythm in patients with AF, but it impairs the sinoatrial node (SAN) function in one-third of AF patien
136           For example, nerve synapses on the sinoatrial node (SAN) impact pacemaking, while synapses
137 d by Ras-related small G proteins, regulates sinoatrial node (SAN) ion channel activity through a mec
138                 Up to 50% of the adult human sinoatrial node (SAN) is composed of dense connective ti
139 ght to confirm our hypothesis that the human sinoatrial node (SAN) is functionally insulated from the
140 ) of the major pacemaker channel HCN4 in the sinoatrial node (SAN) is involved in heart rate regulati
141                                          The sinoatrial node (SAN) maintains a rhythmic heartbeat; th
142 her their presence nor their contribution to sinoatrial node (SAN) pacemaker activity has been invest
143 equence of impaired chronotropic response of sinoatrial node (SAN) pacemaker activity to vagal/parasy
144 ated in controlling automaticity in isolated sinoatrial node (SAN) pacemaker cells, but the potential
145 e sexual dimorphism of genes responsible for sinoatrial node (SAN) pacemaking and signaling pathways
146  in embryonic heart, but their role in adult sinoatrial node (SAN) pacemaking is uncertain.
147 rough K(+) channels are essential for proper sinoatrial node (SAN) pacemaking, but the influence of i
148 ated current, If, plays an important role in sinoatrial node (SAN) pacemaking.
149  However, it is challenging to explore human sinoatrial node (SAN) pathophysiology due to difficulty
150 ces in cardiomyocyte automaticity permit the sinoatrial node (SAN) to function as the leading cardiac
151     Dysfunction of pacemaker activity in the sinoatrial node (SAN) underlies "sick sinus" syndrome (S
152          The heartbeat originates within the sinoatrial node (SAN), a small structure containing <10,
153 pecialized cardiomyocytes located within the sinoatrial node (SAN), and is responsible for originatin
154 which a small anatomical region, such as the sinoatrial node (SAN), can robustly drive electrical act
155                                          The sinoatrial node (SAN), functionally known as the pacemak
156          Reentrant arrhythmias involving the sinoatrial node (SAN), namely SAN reentry, remain one of
157 ine (A(1)R) receptor activation in the mouse sinoatrial node (SAN), the cardiac pacemaker.
158 ction of the pacemaker cardiomyocytes of the sinoatrial node (SAN), the leading pacemaker of the hear
159                                          The sinoatrial node (SAN), the leading pacemaker region, gen
160 ify ion channel transcripts expressed in the sinoatrial node (SAN), the pacemaker of the heart.
161                                          The sinoatrial node (SAN), the primary cardiac pacemaker, co
162           Each heartbeat is triggered by the sinoatrial node (SAN), the primary pacemaker of the hear
163                                          The sinoatrial node (SAN), the primary pacemaker of the hear
164 situ studies indicated that Pitx2 suppresses sinoatrial node (SAN)-specific gene expression, includin
165 ia and ventricles, there is no model for the sinoatrial node (SAN).
166 R) modulates the spontaneous activity of the sinoatrial node (SAN).
167 f the leading pacemaker (LP) site within the sinoatrial node (SAN).
168 ge where the heartbeat originates within the sinoatrial node (SAN).
169 ed by an electrical impulse generated in the sinoatrial node (SAN).
170 tressors is a key homeostatic feature of the sinoatrial node (SAN).
171 by specialized cardiomyocytes located in the sinoatrial node (SAN).
172 te (HR) by inhibiting pacemaker cells in the sinoatrial node (SAN).
173 bx18 give rise to the heart's pacemaker, the sinoatrial node (SAN).
174 of this is the use of optical mapping in the sinoatrial node (SAN): when microelectrode and optical r
175 (ANS), which interacts with receptors on the sinoatrial node (SAN; the heart's primary pacemaker), an
176 uggest that sympathetic reinnervation of the sinoatrial node starts within 6 mo after HTx and strengt
177    We developed a computational model of the sinoatrial node that showed that a loss of SAN cells bel
178 f the atria by increasing its density at the sinoatrial node, the auricles and the major veins attach
179                        During failure of the sinoatrial node, the heart can be driven by an atriovent
180                                  Passing the sinoatrial node, the P-wave developed an initial positiv
181 coupling was investigated by dye transfer in sinoatrial node tissue explants.
182                            RNA sequencing on sinoatrial node tissue lacking Islet-1 established that
183 pecifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting o
184 en by an electrical impulse generated in the sinoatrial node to propagate from atria to ventricles.
185 uction system, extending proximally from the sinoatrial node to the distal Purkinje fibers.
186 ional computerized numerical modeling of the sinoatrial node was conducted to validate the theoretica
187 s is controversial despite the fact that the sinoatrial node was discovered over 100 years ago.
188 d that IRAG is highly expressed in the mouse sinoatrial node where computer modeling predicts that it

 
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