ライフサイエンスコーパス: sinoatrial

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

3 ust expression in the heart, particularly in sinoatrial and atrioventricular nodal regions.

4 distal outflow tract, atrial septum, and in sinoatrial and atrioventricular node.

5 .9 may slow propagation of excitation in the sinoatrial and atrioventricular nodes by shortening the

6 t, unlike ENT1, is virtually absent from the sinoatrial and atrioventricular nodes.

7 electrocardiography or the discovery of the sinoatrial and atrioventricular nodes.

8 , representing a position midway between the sinoatrial and atrioventricular nodes.

9 Much information is encoded in sinoatrial AP waveforms, but both the analysis and the c

10 t I(f) is persistently active throughout the sinoatrial AP, with surprisingly little voltage-dependen

11 e the persistent activity of I(f) during the sinoatrial AP.

12 ntitative analysis and enables comparison of sinoatrial APs by standardizing parameter definitions an

13 parameter that can vary significantly among sinoatrial APs.

14 beats) tachyarrhythmia and bradyarrhythmia (sinoatrial arrest, second- or third-degree atrioventricu

15 HCN dysfunctions lead to sinoatrial block (HCN4), epilepsy (HCN1), and chronic pa

16 pisodes of third-degree atrioventricular and sinoatrial block in every NaV1.5-immunized animal, but n

17 pe of unknown origin and atrioventricular or sinoatrial block lasting >10 seconds (average, 17.9+/-6.

18 tantial increases in atrial premature beats, sinoatrial block, and atrioventricular block, accompanie

19 aptation to exercise by modulating intrinsic sinoatrial cell behavior.

20 a2 AMPK activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate

21 tric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholin

22 Our ability to generate sinoatrial-compatible spontaneous cardiomyocytes from th

23 They also revealed up to five sinoatrial conduction pathways (SACPs), which electrical

24 The sinoatrial conduction pathways acted as a filter for atr

25 tation waves could enter the SAN through the sinoatrial conduction pathways and overdrive suppress th

26 Ch/Iso modulated filtering properties of the sinoatrial conduction pathways by increasing/decreasing

27 xcited via superior, middle, and/or inferior sinoatrial conduction pathways.

28 t SAN activation and to identify specialized sinoatrial conduction pathways.

29 ged sinoatrial node recovery time, increased sinoatrial conduction time, and recurrent sinus pauses.

30 Better sympathetic sinoatrial control improved heart rate responsiveness to

31 er implantation, atrioventricular block, and sinoatrial dysfunction: 0.94% (95% CI: 0.75% to 1.16%) f

32 rial myocardium via superior and/or inferior sinoatrial exit pathways 8.8+/-3.2 mm from the leading p

33 Conduction failure in these sinoatrial exit pathways leads to SAN exit block and is

34 for 2 (or more) narrow superior and inferior sinoatrial exit pathways separated by 12.8+/-4.1 mm.

35 rmal circadian fluctuations and less erratic sinoatrial firing.

36 Both Ca(v)1.2 and Ca(v)1.3 channels mediate sinoatrial L-type currents.

37 pacemaker" current (I(f)) that increases the sinoatrial nodal (SAN) cell membrane diastolic depolariz

38 In wild-type mice, Ang II infusion caused sinoatrial nodal (SAN) cell oxidation by activating NADP

39 Dysregulation of L-type Ca(2+) currents in sinoatrial nodal (SAN) cells causes cardiac arrhythmia.

40 Eleven were found to have an abnormal sinoatrial nodal artery, and 7 of these patients also ha

41 We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled t

42 seizure progression, diverse seizure-induced sinoatrial nodal cell firing patterns during ictal or po

43 ogenic and cardiogenic mechanisms in shaping sinoatrial nodal cell firing patterns, challenging the p

44 y, we utilized a mathematical model of mouse sinoatrial nodal cell pacemaking and an autonomic clampi

45 ted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model c

46 ulum (SR) during diastolic depolarization in sinoatrial nodal cells (SANC) occur even in the basal st

47 are crucial for normal pacemaker function of sinoatrial nodal cells (SANC).

48 release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (SANC).

49 spontaneous diastolic depolarization (DD) of sinoatrial nodal cells (SANCs) that triggers recurrent a

50 ing late diastolic depolarization in cardiac sinoatrial nodal cells (SANCs).

51 s) increases the spontaneous beating rate of sinoatrial nodal cells (SANCs); however, the specific li

52 iological approaches and primary cultures of sinoatrial nodal cells and hippocampal neurons, we show

53 rs (RyRs) during diastolic depolarization of sinoatrial nodal cells augments the terminal depolarizat

54 We determined whether LCRs in rabbit sinoatrial nodal cells require the concurrent membrane d

55 pecifically, while daytime sleep predisposed sinoatrial nodal cells to postictal sinus arrhythmias, n

56 raction) and the spontaneous beating rate of sinoatrial nodal cells were all blunted in RyR2-S2808A+/

57 s in both neonatal atrial myocytes and adult sinoatrial nodal cells.

58 ssociated with ticagrelor were asymptomatic, sinoatrial nodal in origin (66%), and nocturnal.

59 uses, which were predominantly asymptomatic, sinoatrial nodal in origin, and nocturnal and occurred m

60 Ion channels on the surface membrane of sinoatrial nodal pacemaker cells (SANCs) are the proxima

61 e of diastolic depolarization (DD) in rabbit sinoatrial nodal pacemaker cells (SANCs) generate an inw

62 Thus, the biological clock of sinoatrial nodal pacemaker cells, like that of many othe

63 lectively inhibits the funny current (If) in sinoatrial nodal tissue, resulting in a decrease in the

64 ine in situ detection of connexins in rabbit sinoatrial node (a tissue that is particularly rich in f

65 ite dysregulation of PITX2 expression in the sinoatrial node (ectopic activation) and ventricle (redu

66 ted in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4).

67 canine AVJ preparations that did not contain sinoatrial node (n = 10).

68 d indices of sympathovagal modulation of the sinoatrial node (ratio of low-frequency to high-frequenc

69 of the human cardiac conduction system: the sinoatrial node (SAN) and atrioventricular node (AVN), r

70 tructive heart surgery include injury of the sinoatrial node (SAN) and atrioventricular node (AVN), r

71 highly expressed in embryonic myocardium and sinoatrial node (SAN) and is required for cardiac automa

72 Experiments were performed on sinoatrial node (SAN) and latent atrial pacemaker (LAP)

73 Numerous studies implicate the sinoatrial node (SAN) as a participant in atrial arrhyth

74 ane voltage and Ca2+ clocks jointly regulate sinoatrial node (SAN) automaticity.

75 te the activation within the human or canine sinoatrial node (SAN) because they are intramural struct

76 rucial regulatory role in the development of sinoatrial node (SAN) by repressing the expression of Nk

77 olecular and functional properties of native sinoatrial node (SAN) cardiomyocytes.

78 m (ANS) and intrinsic mechanisms that govern sinoatrial node (SAN) cell function.

79 In sinoatrial node (SAN) cells, electrogenic sodium-calcium

80 t these sites and how this relates to normal sinoatrial node (SAN) development remain uncharacterized

81 Mechanisms for human sinoatrial node (SAN) dysfunction are poorly understood

82 Although sinoatrial node (SAN) dysfunction is a hallmark of human

83 Sinoatrial node (SAN) dysfunction is commonly associated

84 polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of whi

85 lure (HF) is frequently accompanied with the sinoatrial node (SAN) dysfunction, which causes tachy-br

86 primary pacemaker area of the intact rabbit sinoatrial node (SAN) exhibits robust positive labeling

87 ythm in patients with AF, but it impairs the sinoatrial node (SAN) function in one-third of AF patien

88 For example, nerve synapses on the sinoatrial node (SAN) impact pacemaking, while synapses

89 d by Ras-related small G proteins, regulates sinoatrial node (SAN) ion channel activity through a mec

90 Up to 50% of the adult human sinoatrial node (SAN) is composed of dense connective ti

91 ght to confirm our hypothesis that the human sinoatrial node (SAN) is functionally insulated from the

92 ) of the major pacemaker channel HCN4 in the sinoatrial node (SAN) is involved in heart rate regulati

93 The sinoatrial node (SAN) maintains a rhythmic heartbeat; th

94 her their presence nor their contribution to sinoatrial node (SAN) pacemaker activity has been invest

95 equence of impaired chronotropic response of sinoatrial node (SAN) pacemaker activity to vagal/parasy

96 ated in controlling automaticity in isolated sinoatrial node (SAN) pacemaker cells, but the potential

97 e sexual dimorphism of genes responsible for sinoatrial node (SAN) pacemaking and signaling pathways

98 in embryonic heart, but their role in adult sinoatrial node (SAN) pacemaking is uncertain.

99 rough K(+) channels are essential for proper sinoatrial node (SAN) pacemaking, but the influence of i

100 ated current, If, plays an important role in sinoatrial node (SAN) pacemaking.

101 However, it is challenging to explore human sinoatrial node (SAN) pathophysiology due to difficulty

102 ces in cardiomyocyte automaticity permit the sinoatrial node (SAN) to function as the leading cardiac

103 Dysfunction of pacemaker activity in the sinoatrial node (SAN) underlies "sick sinus" syndrome (S

104 The heartbeat originates within the sinoatrial node (SAN), a small structure containing <10,

105 pecialized cardiomyocytes located within the sinoatrial node (SAN), and is responsible for originatin

106 which a small anatomical region, such as the sinoatrial node (SAN), can robustly drive electrical act

107 The sinoatrial node (SAN), functionally known as the pacemak

108 Reentrant arrhythmias involving the sinoatrial node (SAN), namely SAN reentry, remain one of

109 ine (A(1)R) receptor activation in the mouse sinoatrial node (SAN), the cardiac pacemaker.

110 ction of the pacemaker cardiomyocytes of the sinoatrial node (SAN), the leading pacemaker of the hear

111 The sinoatrial node (SAN), the leading pacemaker region, gen

112 ify ion channel transcripts expressed in the sinoatrial node (SAN), the pacemaker of the heart.

113 The sinoatrial node (SAN), the primary cardiac pacemaker, co

114 Each heartbeat is triggered by the sinoatrial node (SAN), the primary pacemaker of the hear

115 The sinoatrial node (SAN), the primary pacemaker of the hear

116 situ studies indicated that Pitx2 suppresses sinoatrial node (SAN)-specific gene expression, includin

117 bx18 give rise to the heart's pacemaker, the sinoatrial node (SAN).

118 f the leading pacemaker (LP) site within the sinoatrial node (SAN).

119 ge where the heartbeat originates within the sinoatrial node (SAN).

120 ia and ventricles, there is no model for the sinoatrial node (SAN).

121 R) modulates the spontaneous activity of the sinoatrial node (SAN).

122 ed by an electrical impulse generated in the sinoatrial node (SAN).

123 tressors is a key homeostatic feature of the sinoatrial node (SAN).

124 by specialized cardiomyocytes located in the sinoatrial node (SAN).

125 te (HR) by inhibiting pacemaker cells in the sinoatrial node (SAN).

126 of this is the use of optical mapping in the sinoatrial node (SAN): when microelectrode and optical r

127 (ANS), which interacts with receptors on the sinoatrial node (SAN; the heart's primary pacemaker), an

128 dly rectifying K+ (GIRK or KACh) channels of sinoatrial node and atria play a major role in beat-to-b

129 shown at birth to be present throughout the sinoatrial node and atrial muscle, however, at one month

130 ls is required for proper hearing as well as sinoatrial node and brain function.

131 ty of cell types and distribution within the sinoatrial node and cell-cell interactions add complexit

132 ntify Islet-1 as a novel marker of the adult sinoatrial node and do not provide evidence for Islet-1(

133 izes the leading pacemaker region within the sinoatrial node and hence is crucial for stable heart ra

134 the HCN1 protein is highly expressed in the sinoatrial node and is colocalized with HCN4, the main s

135 ardiac myocytes and specialized cells in the sinoatrial node and the conduction system.

136 els of MiRP1 and HCN subunits in the cardiac sinoatrial node and the contribution of pacemaker channe

137 The sinoatrial node and the ventricle of the heart receive s

138 ocal gene expression to resemble that of the sinoatrial node and unleashed automaticity originating a

139 Pacemaker cardiomyocytes that create the sinoatrial node are essential for the initiation and mai

140 ) hearts the focus ultimately shifted to the sinoatrial node at a very prolonged cycle length (initia

141 Here, we review the latest findings on sinoatrial node automaticity and discuss the physiologic

142 t density contributes to the acceleration of sinoatrial node automaticity and explains, in part, the

143 Sinoatrial node automaticity was slowed in treated group

144 recorded from isolated papillary muscle and sinoatrial node by microelectrode techniques.

145 current appearing in the Noble model of the sinoatrial node cell in the mammalian heart.

146 r evaluated in rabbit isolated patch-clamped sinoatrial node cells (n = 21), where we found that 5 mu

147 Spontaneous beating of rabbit sinoatrial node cells (SANCs) is controlled by cAMP-medi

148 neath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic

149 ct in concert with ion channels to confer on sinoatrial node cells (SANCs) their status of dominance

150 roughly periodic LCRs in depolarized rabbit sinoatrial node cells (SANCs).

151 caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous

152 geneity of the electrical activity of single sinoatrial node cells as well as that of the intact sino

153 m cell differentiation cultures enriches for sinoatrial node cells exhibiting a functional pacemaker

154 Spontaneous action potentials of sinoatrial node cells from pregnant mice exhibited highe

155 and the targeted delivery of therapeutics to sinoatrial node cells in vivo using antibody-drug conjug

156 The electrical activity of sinoatrial node cells is heterogeneous.

157 intracellular cAMP levels were unchanged in sinoatrial node cells of pregnant mice.

158 In sinoatrial node cells of the heart, beating rate is cont

159 ted inward current similar to the If seen in sinoatrial node cells of the heart.

160 etal and human pluripotent stem cell-derived sinoatrial node cells to reveal that they consist of thr

161 (as measured by cell capacitance) of rabbit sinoatrial node cells was investigated using the whole-c

162 n of pacemaker mechanisms in single isolated sinoatrial node cells, explanted beating sinoatrial node

163 on of spontaneous action potential firing in sinoatrial node cells.

164 ergically stimulated ion channels in cardiac sinoatrial node cells.

165 tes to the pacemaker current (I(f)) in human sinoatrial node cells.

166 .0 pA/pF; P, -28.6+/-2.9 pA/pF; P=0.0002) in sinoatrial node cells.

167 the slope of the diastolic depolarization of sinoatrial node cells.

168 ysis that Cx43 protein expression within the sinoatrial node decreased with age; however, the express

169 uch as Shox2 and Tbx3, that are required for sinoatrial node development.

170 r conduction block and arrhythmias caused by sinoatrial node dysfunction are clinically important and

171 Sinoatrial node dysfunction associated with CPVT may inc

172 Clinical studies have shown that sinoatrial node dysfunction occurs at the highest incide

173 d cation channels may protect the heart from sinoatrial node dysfunction, secondary arrhythmia of the

174 hmias: sinus pauses and bradycardia indicate sinoatrial node dysfunction, whereas preexcitation and a

175 ation and miR-106b-25 heterozygosity develop sinoatrial node dysfunction.

176 mechanisms; underlies time-of-day changes in sinoatrial node excitability/intrinsic heart rate; and l

177 P maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those obser

178 h-frequency ratio [P=0.03]) and less erratic sinoatrial node firing (eg, lower Poincare ratio [P=0.02

179 The age-dependent reduction in sinoatrial node function was not associated with changes

180 of conduction abnormalities and compromised sinoatrial node function which could lead to increased r

181 vagal activity, baroreceptor responses, and sinoatrial node function.

182 x2 regulates microRNAs (miRs) to repress the sinoatrial node genetic program.

183 onic parasympathetic neurons innervating the sinoatrial node in control and HF dogs (both, n=8).

184 beta-adrenergic receptor stimulation of the sinoatrial node in intact dogs is markedly blunted when

185 h incidence of bradycardia suggests possible sinoatrial node involvement.

186 We show that the sinoatrial node is compartmentalized, with a core of pac

187 y definition, that pacemaker function of the sinoatrial node is compromised during aging.

188 lular and molecular composition of the human sinoatrial node is not resolved.

189 The sinoatrial node is the main impulse-generating tissue in

190 In this study, we have assessed the roles of sinoatrial node L-type Ca(v)1.3 (alpha(1D)) Ca(2+) chann

191 ectrical signal is known to originate in the sinoatrial node myocyte, but exactly what role Ca plays

192 Sinoatrial node myocytes (SAMs) act as cardiac pacemaker

193 ow that depressed excitability of individual sinoatrial node myocytes (SAMs) contributes to reduction

194 Sinoatrial node myocytes act as cardiac pacemaker cells

195 g of the intrinsic pacemaker activity of the sinoatrial node of the heart, which results from electri

196 +) cells in the right atrium coexpressed the sinoatrial node pacemaker cell marker HCN4.

197 This sinoatrial node pacemaker cell surface marker is highly

198 cell surface marker to identify and isolate sinoatrial node pacemaker cells has been reported.

199 Our study identifies a host of sinoatrial node pacemaker markers including MYH11, BMP4,

200 In an ex vivo murine sinoatrial node preparation, addition of the K(Ca)1.1 an

201 ted sinoatrial node cells, explanted beating sinoatrial node preparation, telemetric in vivo electroc

202 nitiates early in development, represses the sinoatrial node program and pacemaker activity on the le

203 by bradycardia, sinus dysrhythmia, prolonged sinoatrial node recovery time, increased sinoatrial cond

204 the greatest density of innervation near the sinoatrial node region (P < 0.05, n = 6).

205 odissection were isolated, including: Zone I-sinoatrial node region; Zone II-atrioventricular node/Hi

206 The sinoatrial node regulates the heart rate throughout life

207 uggest that sympathetic reinnervation of the sinoatrial node starts within 6 mo after HTx and strengt

208 We developed a computational model of the sinoatrial node that showed that a loss of SAN cells bel

209 coupling was investigated by dye transfer in sinoatrial node tissue explants.

210 RNA sequencing on sinoatrial node tissue lacking Islet-1 established that

211 pecifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting o

212 en by an electrical impulse generated in the sinoatrial node to propagate from atria to ventricles.

213 uction system, extending proximally from the sinoatrial node to the distal Purkinje fibers.

214 ional computerized numerical modeling of the sinoatrial node was conducted to validate the theoretica

215 s is controversial despite the fact that the sinoatrial node was discovered over 100 years ago.

216 d that IRAG is highly expressed in the mouse sinoatrial node where computer modeling predicts that it

217 Given that other biological (e.g., sinoatrial node) and artificial systems display phase-lo

218 ctive blocker of the I(funny) channel in the sinoatrial node) on heart rate, quality of life (QOL), a

219 We found that cardiomyocytes of the atria, sinoatrial node, and ventricular conduction system expre

220 within regions of the heart that become the sinoatrial node, atrioventricular node, and bundle of Hi

221 ugh the components of the CCS, including the sinoatrial node, atrioventricular node, His bundle, bund

222 opagation of the action potential across the sinoatrial node, from the initiation point to the crista

223 [Ca(2+)]i release and Ca(2+) handling in the sinoatrial node, impaired pacemaker activity and symptom

224 f the atria by increasing its density at the sinoatrial node, the auricles and the major veins attach

225 During failure of the sinoatrial node, the heart can be driven by an atriovent

226 Passing the sinoatrial node, the P-wave developed an initial positiv

227 ession and network analysis identified novel sinoatrial node-enriched genes and predicted that the tr

228 CN4 for the central pacemaker process in the sinoatrial node.

229 The AVJ is a primary backup pacemaker to the sinoatrial node.

230 e ganglia, respectively, that project to the sinoatrial node.

231 may mask intrinsic fractal behaviour of the sinoatrial node.

232 and peripheral cells that make up the native sinoatrial node.

233 right atrial foci, especially those near the sinoatrial node.

234 e wall, corresponding to the location of the sinoatrial node.

235 otein was not expressed in the centre of the sinoatrial node.

236 lowering agent that acts specifically on the sinoatrial node.

237 of ionic currents in pacemaker cells of the sinoatrial node.

238 ial node cells as well as that of the intact sinoatrial node.

239 adycardia, consistent with AC9 expression in sinoatrial node.

240 It also is present in areas within the sinoatrial node.

241 aneous firing rate of pacemaker cells in the sinoatrial node.

242 role in generating pacemaker activity of the sinoatrial node.

243 s from RIalpha-icKO mice but not in atria or sinoatrial node.

244 discovered nonfiring pacemaker cells in the sinoatrial node.

245 wave of electrical activity initiated at the sinoatrial node.

246 unction, with initial, larger effects on the sinoatrial node.

247 nscriptional regulator within the developing sinoatrial node.

248 properties of pacemaker myocytes in the aged sinoatrial node.

249 sistently Islet-1 mRNA was detected in human sinoatrial node.

250 er-law behavior comparable to those of human sinoatrial node.

251 in isolated guinea pig spontaneously beating sinoatrial node/atrial preparations.

252 beta-adrenergic regulation of heart rate and sinoatrial pacemaker activity in mice lacking Ca(v)1.3 c

253 A single isolated sinoatrial pacemaker cell presents intrinsic interbeat i

254 quency of pacemaker potentials from isolated sinoatrial pacemaker cells in the presence of endogenous

255 ffect of current fluctuations on the IBIs of sinoatrial pacemaker cells.

256 node and is colocalized with HCN4, the main sinoatrial pacemaker channel isoform.

257 chronotropic response to sympathomimetics of sinoatrial pacemaker myocytes under conditions of specif

258 which organized activation emanated from the sinoatrial pacemaker region.

259 ined how these properties of Ca(v)1.3 affect sinoatrial pacemaking in a mathematical model.

260 heart rate (rgs6 and hcn4); and the risk of sinoatrial pauses and arrests (hcn4).

261 right vagosympathetic trunks innervated the sinoatrial plexus proximal to their entry into the heart

262 were contacted by fiber varicosities in the sinoatrial plexus than in the atrioventricular plexus af

263 The pacemaker converges to the sinoatrial region during development and comprises fewer

264 oepicardium, which develops posterior to the sinoatrial region of the looping-stage heart.

265 ces of early sympathetic and parasympathetic sinoatrial reinnervation, as well as explored indirect e

266 hin the brain and heart set daily rhythms in sinoatrial (SA) and atrioventricular (AV) node activity,

267 The arrhythmia included sinoatrial (SA) block, sinus arrest, 2 degrees and 3 deg

268 Sinoatrial (SA) nodal cells were identified in cardiac t

269 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

270 from the spontaneous rhythmic excitation of sinoatrial (SA) node cells.

271 on entry through L-type Ca2+ channels in the sinoatrial (SA) node contributes to pacemaker activity,

272 ontaneous activity of pacemaker cells in the sinoatrial (SA) node controls heart rate under normal ph

273 retation (mosaic model) of the makeup of the sinoatrial (SA) node has been proposed to explain the ch

274 on enzymatically isolated myocytes from the sinoatrial (SA) node, right and left atria, right and le

275 nt in the myocytes of the ventricles and the sinoatrial (SA) node.

276 x5 expression is restricted to the posterior sinoatrial segments of the heart, consistent with the ti

277 sceptibility to AF was evaluated in isolated sinoatrial tissue and in vivo in mice.

278 ed at the venous pole in a plexus around the sinoatrial valve; mean total number of cells was 197 +/-

279 d channel 4, were located in the base of the sinoatrial valves, and this region was densely innervate

280 located in a ganglionated plexus around the sinoatrial valves.