ライフサイエンスコーパス: atrial myocyte

1 orating a detailed ionic-current model of an atrial myocyte.

2 vations about the spread of Ca(2+) within an atrial myocyte.

3 nt within the three-dimensional volume of an atrial myocyte.

4 ptor clusters within a specific z disk of an atrial myocyte.

5 ecular and electrophysiological phenotype of atrial myocytes.

6 lexes among different SK channel subunits in atrial myocytes.

7 were altered consistently in ST8sia2((-/-)) atrial myocytes.

8 nd outward currents during repolarization in atrial myocytes.

9 of SK2 channels in cardiac repolarization in atrial myocytes.

10 ith the Cav3.1 channel in both HEK cells and atrial myocytes.

11 nt gap junction protein that is expressed in atrial myocytes.

12 monstrated TREK-1 protein in the membrane of atrial myocytes.

13 gnificantly smaller in +LMN compared to -LMN atrial myocytes.

14 alpha-adrenergic and cholinergic signals in atrial myocytes.

15 tois by specialized secretory cells, such as atrial myocytes.

16 ling of Kv1.5 in the HL-1 immortalized mouse atrial myocytes.

17 and an attenuation of I(Ca,L) in the canine atrial myocytes.

18 preparations, and patch clamping in isolated atrial myocytes.

19 s can trigger arrhythmias in ventricular and atrial myocytes.

20 obal Ca2+ increase and muscle contraction in atrial myocytes.

21 tion of RyR2 clusters in rat and ventricular atrial myocytes.

22 .87 microm in ventricular and 1.69 microm in atrial myocytes.

23 icular myocytes and estimated 0.97 microm in atrial myocytes.

24 e voltage-dependent activation of I(Ca,L) in atrial myocytes.

25 (PE) on L-type Ca2+ current (I(Ca,L)) in cat atrial myocytes.

26 central release of Ca(2+) in this subset of atrial myocytes.

27 is the predominant IP3R isoform expressed in atrial myocytes.

28 e and uptake in intact and permeabilized cat atrial myocytes.

29 were not different in WT and IP3R2-deficient atrial myocytes.

30 neous Ca2+ release events in IP3R2-deficient atrial myocytes.

31 diversity of local Ca(2+) signalling in rat atrial myocytes.

32 oline (ACh) on intracellular NO (NOi) in cat atrial myocytes.

33 te exposure to thyroid hormone (T(3)) on cat atrial myocytes.

34 to action potential repolarization of human atrial myocytes.

35 (2)-adrenergic receptor (AR) agonists in cat atrial myocytes.

36 with a loss of carbachol-induced current in atrial myocytes.

37 tivated, or T-type Ca(2+), channel in murine atrial myocytes.

38 lation of L-type Ca(2+) current (I(Ca,L)) in atrial myocytes.

39 icantly inhibited ICl,vol in most guinea-pig atrial myocytes.

40 patches from acutely dissociated guinea-pig atrial myocytes.

41 nt atrial pacemaker cells but not in working atrial myocytes.

42 key component of parasympathetic synapses on atrial myocytes.

43 ed in discrete bundles that appeared to abut atrial myocytes.

44 s a low voltage-activated calcium channel in atrial myocytes.

45 duced delayed afterdepolarizations (DADs) in atrial myocytes.

46 (ANP) is present in caveolae of in situ rat atrial myocytes.

47 d atrial myocytes and of freshly dissociated atrial myocytes.

48 shown that SR Ca content is increased in old atrial myocytes.

49 rinic stimulation of native GIRK currents in atrial myocytes.

50 n ventricular myocytes were also observed in atrial myocytes.

51 dine block of IKr and IKur currents in human atrial myocytes.

52 regulation controlling the repolarization of atrial myocytes.

53 Ca(2+) release in subsarcolemmal domains of atrial myocytes.

54 ve changes in the calcium handling system of atrial myocytes.

55 anisms of cardiac alternans in single rabbit atrial myocytes.

56 from the IP3 R2 in the peripheral domains of atrial myocytes.

57 ar stress-sensitive current (Ishear ) in rat atrial myocytes.

58 id communication and coordinate responses of atrial myocytes.

59 pe-mediated Ca(2+) current in EHD3-deficient atrial myocytes.

60 iggered calcium waves (TCWs) in isolated dog atrial myocytes.

61 also had opposing effects on ICa,L in human atrial myocytes.

62 ANP had any effect on Na(+) current in mouse atrial myocytes.

63 1 expression in enzymatically isolated human atrial myocytes.

64 Ca2+ signaling in isolated rabbit and human atrial myocytes.

65 region of the SHF gives rise to both OFT and atrial myocytes.

66 lonal line of conditionally immortalized rat atrial myocytes.

67 ed ACs are functionally active in guinea-pig atrial myocytes.

68 K,ACh) is opposite to its effect on I(K1) in atrial myocytes.

69 ependent on CaMKII) that regulates I(CaL) in atrial myocytes.

70 (2+) release were recorded in isolated human atrial myocytes.

71 channel membrane targeting and regulation in atrial myocytes.

72 potential duration was prolonged in 6.1-gKO atrial myocytes, absent of changes in other ion channel

73 We conclude that in cat atrial myocytes, ACh stimulates NOi release from local s

74 Ventricular myocytes and tubulated atrial myocytes additionally exhibited early afterdepola

75 WT and IP3R2-deficient atrial myocytes also showed a significant and very simil

76 The canonical atrial myocyte (AM) is characterized by sparse transvers

77 nized transverse tubules (T-tubules) such as atrial myocytes (AMs).

78 luciferase activity in cultured neonatal rat atrial myocytes, an effect that was increased to 8-9-fol

79 PDE4 is expressed in human atrial myocytes and accounts for approximately 15% of to

80 KACh) deactivation kinetics in both neonatal atrial myocytes and adult sinoatrial nodal cells.

81 channels (SK, KCa 2) are expressed in human atrial myocytes and are responsible for shaping atrial a

82 minated both CaT and APD alternans in single atrial myocytes and atrial T-wave alternans at the whole

83 ecreased L-type calcium current (I(Ca,L)) in atrial myocytes and decreased atrial contractility.

84 S107 reduced the diastolic SR Ca2+ leak in atrial myocytes and decreased burst pacing-induced AF in

85 Electrotonic coupling between atrial myocytes and Fbs may contribute to the formation

86 s the timing of parasympathetic influence on atrial myocytes and heart rate in mice.

87 eceptor when tested in cultured neonatal rat atrial myocytes and HeLa cells.

88 2+) signals ([Ca(2+)](Nuc)) in permeabilized atrial myocytes and in isolated cardiac nuclei.

89 via pertussis toxin-sensitive G proteins in atrial myocytes and in many neuronal cells.

90 of SCaEs and delayed afterdepolarizations in atrial myocytes and intact atria and prevented induction

91 potassium channel forms the IKur current in atrial myocytes and is functionally altered by coexpress

92 NP colocalize at the plasmalemma of cultured atrial myocytes and of freshly dissociated atrial myocyt

93 tes the I(Kur) repolarizing current in human atrial myocytes and regulates vascular tone in multiple

94 We used isolated rat atrial myocytes and related changes in their subcellular

95 nside the cells; they are expressed in human atrial myocytes and responsible for shaping atrial actio

96 the gamma(6) subunit is highly expressed in atrial myocytes and that it is capable of acting as a ne

97 the density of K+ currents in left and right atrial myocytes and the density of delayed rectifier K+

98 Ca(2+) spark frequency in atrial myocytes and the open probability of single RyR2

99 nt which was found to be absent in tubulated atrial myocytes and ventricular myocytes.

100 transfection of mouse C2C12 myoblasts, HL-1 atrial myocytes, and c-kit(+) cardiac progenitor cells d

101 welling-activated Cl- currents in guinea pig atrial myocytes, and Ca(2+)-activated Cl- currents in ca

102 g in high sensor expression in arterial ECs, atrial myocytes, and cardiac Purkinje fibers.

103 nt (Ik(ur)), a major repolarizing current in atrial myocytes, and regulating the resting membrane pot

104 Ankyrin-B is expressed in atrial myocytes, and we demonstrate its requirement for

105 etected in approximately 40 % of adult mouse atrial myocytes, and when expressed, the density of this

106 These experimental designs tested whether atrial myocyte ANP-RB colocalizes at the plasmalemma and

107 mANP (10-100 nmol/L) had opposing effects on atrial myocyte AP morphology and ICa,L.

108 Atrial myocytes are continuously exposed to mechanical f

109 trated that the functions of SK2 channels in atrial myocytes are critically dependent on the normal e

110 e properties of Ito,f and Iss in adult mouse atrial myocytes are similar to those of the analogous cu

111 Atrial myocytes are subjected to shear stress during the

112 T-current density that normally results when atrial myocytes are treated with insulin-like growth fac

113 an in the ventricle, t-tubules also exist in atrial myocytes as a network of transverse invaginations

114 g) was studied in isolated fluo-3-loaded rat atrial myocytes at 22 and 37 degrees C using rapid confo

115 ctance is essentially abolished in SUR1(-/-) atrial myocytes but is normal in SUR1(-/-) ventricular m

116 IK,ACh in uninfected and freshly dissociated atrial myocytes but the effect was larger and more consi

117 ould be stimulated in the central regions of atrial myocytes by application of 2.5 mM caffeine.

118 ediated Ca2+ influx in isolated canine right atrial myocytes by approximately 60%, but had no signifi

119 in adult isolated canine ventricular and and atrial myocytes by using whole-cell and perforated-patch

120 and APs were recorded from rabbit and human atrial myocytes by whole-cell-patch clamp.

121 etion also reduced Kv currents in male mouse atrial myocytes, by >45% (P < 0.001).

122 ted in the HL-1 cell line derived from mouse atrial myocytes, by using small interfering RNA knockdow

123 oach successfully reproduces key features of atrial myocyte Ca(2+) signaling observed using confocal

124 ABSTRACT: In atrial myocytes Ca(2+) release during excitation-contrac

125 ERCA function was altered to reproduce human atrial myocyte Ca2+ transients.

126 Ferret atrial myocytes can display an E-4031-sensitive current

127 helin-1 (ET-1) stimulation of wild-type (WT) atrial myocytes caused an increase in basal [Ca2+]i, an

128 sed the increase in K+ current of guinea pig atrial myocytes caused by 100 microM adenosine (259 +/-

129 ed in the cytoplasmic microdomain underlying atrial myocyte caveolae may be the activation of cGMP-de

130 ification and [K+]o sensitivity in the mouse atrial myocyte cell line, AT-1 cells.

131 We established atrial myocyte cell lines expressing siRNA against desmo

132 tial distribution of Cav1.3 Ca2+ channels in atrial myocytes compared with ventricles.

133 .5 contribute to distinct K+ currents in rat atrial myocytes demonstrates that Kv1.2 and Kv1.5 also d

134 e ventricle and atrium but also vary between atrial myocytes depending on subcellular structure and e

135 ivation of Ca(2+) current was 40 to 70 ms in atrial myocytes (depending on holding potential) so this

136 In HF atrial myocytes diastolic [Ca(2+)]i was increased, actio

137 We conclude that rat atrial myocytes display a predetermined spatiotemporal p

138 Moreover, ankyrin-B(+/-) atrial myocytes display shortened action potentials, con

139 Ca(2+) signals in indo-1- and fluo-4-loaded atrial myocytes during electrical pacing.

140 e centripetal Ca(2+) waves that occur within atrial myocytes during excitation-contraction coupling,

141 enting some of the Ang II-induced changes in atrial myocyte electrophysiology and preventing fibrosis

142 of Ca(2+) alternans in field-stimulated cat atrial myocytes employing fast two-dimensional fluoresce

143 In intact cat atrial myocytes, endothelin (ET-1) increased basal [Ca(2

144 In approximately 30 % of the atrial myocytes examined, 8-Br-cAMP increased macroscopi

145 te EHD3 as a key player in the regulation of atrial myocyte excitability and cardiac conduction.

146 KEY POINTS: In atrial myocytes excitation-contraction coupling is strik

147 S6 in G protein inactivation, RGS6-deficient atrial myocytes exhibited a significant reduction in the

148 investigate whether intracaveolar ANP of rat atrial myocytes exists within caveolae bound to type B A

149 nctions as a dominant negative, and from P15 atrial myocytes exposed to (1 microM) antisense oligodeo

150 urrents were attenuated significantly in rat atrial myocytes exposed to AsODNs targeted against Kv4.2

151 Atrial myocytes express three different gap junction cha

152 In this study, treatment of HL-1 atrial myocytes expressing Kv1.5-GFP with the class I an

153 In cultured adult rabbit left atrial myocytes, expression of S140G-IKs shortened actio

154 As with acetylcholine-activated current in atrial myocytes, external Cs+ blocked inward but not out

155 Immunostaining atrial myocytes for type II ryanodine receptors (RyRs) r

156 Atrial myocytes, for example, coexpress connexin (Cx) 40

157 ce microscopy applied to primary cultures of atrial myocytes from adult rats and to freshly dissociat

158 Incubation of atrial myocytes from AF patients (but not controls) with

159 oltage-gated outward K+ current densities in atrial myocytes from AF patients demonstrates the need t

160 Whole-cell patch-clamp studies of atrial myocytes from Akita mice exhibited a markedly dec

161 These effects were greater in left atrial myocytes from Ang II-treated NPR-C(-/-) mice.

162 In vitro I-1c gene transfer in isolated left atrial myocytes from both pigs and rats increased calciu

163 excitation-contraction coupling in isolated atrial myocytes from cat heart.

164 nts (I(Ca,L)) recorded from single, isolated atrial myocytes from Cav1.3(-/-) mice showed a significa

165 Atrial myocytes from FKBP12.6-/- mice exhibited spontane

166 spark frequency, SR Ca(2+) leak, and DADs in atrial myocytes from FKBP12.6-/-:S2814A mice compared wi

167 ion, the data support the hypothesis that in atrial myocytes from hearts with left ventricular failur

168 is showed that miR-21 was expressed in human atrial myocytes from patients in sinus rhythm and that i

169 gical K(2P)3.1 inhibition prolonged APD90 in atrial myocytes from patients with chronic AF to values

170 I KACh, attenuated in atrial myocytes from SREBP-1 knockout mice, was stimulat

171 rominently in late cardiac repolarization in atrial myocytes from the heterozygous and homozygous nul

172 ced spontaneous diastolic Ca(2+) releases in atrial myocytes from the patients with SR that were abol

173 blotting) in tissue homogenates and isolated atrial myocytes from the right atrial appendage (RAA) of

174 n of GIRK1, SREBP-1, and I(KAch) activity in atrial myocytes from these mice to levels in wild-type m

175 isoprenaline-mediated regulation of I Ks in atrial myocytes from transgenic but not WT littermates.

176 (ICa,L), and Na(+) current were recorded in atrial myocytes from wild-type or natriuretic peptide re

177 Using single atrial myocytes from young and old Welsh Mountain sheep,

178 Atrial myocytes generally lack transverse tubules; howev

179 The results indicate that in atrial myocytes glycolysis regulates Ca(2+) release from

180 Isolated hypoxic atrial myocytes had 43% fewer dense surface secretory gr

181 To represent the system, a human atrial myocyte (hAM) coupled to a variable number of Fbs

182 Atrial myocytes have two functionally separate Ca2+ rele

183 nges in other ion channel gene expression or atrial myocyte hypertrophy.

184 or Ca(2+)-stimulated AC in the regulation of atrial myocyte I(CaL).

185 In atrial myocytes immunocytochemistry has shown two groups

186 granules and degenerative myelin figures in atrial myocytes; immunogold studies localized Rab1a to t

187 In 11 rabbit atrial myocytes in which EADs were generated either by i

188 In contrast to atrial myocytes, in mink lung epithelial cells, in which

189 of gene expression similar to that of adult atrial myocytes, including expression of alpha-cardiac m

190 regular-type action potentials of PMCA1(cko) atrial myocytes increased significantly under Ca(2+) ove

191 tion and early after-depolarization in human atrial myocytes, increasing vulnerability to stress-prov

192 Recent experiments in atrial myocytes indicate that withdrawal of cholinergic

193 pendent process, with rapid pacing in canine atrial myocytes inducing oxidative injury through the in

194 Similar results were obtained in +LMN atrial myocytes infected with Adv-FRNK.

195 response to atrial stretch is secreted from atrial myocytes into the circulation, where it stimulate

196 ervations support the hypothesis that in rat atrial myocytes, intracaveolar ANP is bound to ANP-RB, a

197 trate that generation of oxidative injury in atrial myocytes is a frequency-dependent process, with r

198 The atrial natriuretic peptide secreted by atrial myocytes is a major adipogenic factor operating a

199 r the inwardly rectifying K+ current IK1, in atrial myocytes is affected by the expression of Kv4.2W3

200 that RyR2-mediated diastolic SR Ca2+ leak in atrial myocytes is associated with AF in CPVT mice.

201 In type 2 IP3 R (IP3 R2) knockout atrial myocytes, Ishear was 10-20% of that in wild-type

202 t of AF on human I(Ca), we compared I(Ca) in atrial myocytes isolated from 42 patients in normal sinu

203 Voltage-clamp studies on atrial myocytes isolated from adult and postnatal day 15

204 GIRK1 appeared intracellular in atrial myocytes isolated from GIRK4 knockout mice and wa

205 nt densities are attenuated significantly in atrial myocytes isolated from P15 and adult Kv2.1N216Fla

206 tward K+ current densities in left and right atrial myocytes isolated from patients in chronic AF, re

207 was a significant diastolic SR Ca2+ leak in atrial myocytes isolated from the CPVT mouse models.

208 veal that Ito,f is selectively eliminated in atrial myocytes isolated from transgenic mice expressing

209 In canine atrial myocytes, isoprenaline (1 microM) consistently re

210 strikingly different from ventricle because atrial myocytes lack a transverse tubule membrane system

211 In many species atrial myocytes lack a transverse tubule system, dividin

212 The finding that cat atrial myocytes lack t-tubules demonstrates the function

213 Cat atrial myocytes lack transverse tubules and contain sarc

214 acilitating the propagation of Ca2+ waves in atrial myocytes lacking t-tubular system and provide the

215 Atrial myocytes, lacking t-tubules, have two functionall

216 In embryonic chick atrial myocytes, lipid lowering by culture in lipoprotei

217 cell patch clamping, in vitro tachypacing of atrial myocytes, lucigenin chemiluminescence assay, immu

218 lated areas and markedly depressed in viable atrial myocytes near the ablation zones (group 1).

219 When primary cultures of Pam (0-Cre-cKO/cKO) atrial myocytes (no Cre recombinase, PAM floxed) were tr

220 These results indicate that in atrial myocytes, NO released by selective beta(2)-AR sti

221 ndant apoJ mRNA and protein are expressed in atrial myocytes; no expression is detected in ventricula

222 om adult rats and to freshly dissociated rat atrial myocytes (not cultured).

223 In human atrial myocytes obtained from patients in sinus rhythm,

224 smic reticulum Ca(2+)-leak were increased in atrial myocytes of miR-106b-25(-/-) mice.

225 due to enhanced steady-state inactivation in atrial myocytes of patients with SDB consistent with sig

226 eported that short-term (2 h) plating of cat atrial myocytes on the extracellular matrix protein, lam

227 ormal excitation-contraction coupling in cat atrial myocytes, only Ca(2+) release from the j-SR is di

228 We conclude that in cat atrial myocytes PE acts via alpha1-ARs coupled to PTX-in

229 Studies were performed on acutely isolated atrial myocytes plated on uncoated coverslips (LMN) or c

230 Next, we show that the increased SR load in atrial myocytes predisposes these cells to subcellular C

231 ssion of exogenous PAM in Pam (Myh6-cKO/cKO) atrial myocytes produced a dose-dependent rescue of proA

232 ed in part on a previous model of the rabbit atrial myocyte published by our group and was motivated

233 Moreover, loss of ankyrin-B in atrial myocytes results in decreased Ca(v)1.3 expression

234 ecordings from isolated adult (C57BL6) mouse atrial myocytes reveal the presence of two prominent Ca2

235 electron micrographs of thin sections of rat atrial myocytes revealed a fraction of dystrophin molecu

236 -SR ([Ca(2+) ]SR ; fluo-5N) Ca(2+) in rabbit atrial myocytes revealed that Ca(2+) release from j-SR r

237 Immunocytochemical analysis of cultured rat atrial myocytes revealed that T-cadherin and caveolin ha

238 y, adenoviral expression of SREBP-1 in Akita atrial myocytes reversed the impaired I(KAch) to levels

239 ctedly leads to increased outward current in atrial myocytes, shortens atrial action potentials, and

240 Therefore all G protein-coupled receptors in atrial myocytes should be able to activate IK,ACh.

241 Electron micrographs of atrial myocytes show peripheral SR cisternae in close pr

242 tion (100 nM isoproterenol), only Casq2(-/-) atrial myocytes showed pacing-induced self-sustained rep

243 e SK channels are predominantly expressed in atrial myocytes, specific ligands of the different isofo

244 Insulin treatment of cultured atrial myocytes stimulated GIRK1 expression 2.68+/-0.12-

245 work to establish a mechanistic link between atrial myocyte structural remodeling in HF and AF.

246 In single rabbit atrial myocytes, suppression of Ca(2+) -activated Cl(-)

247 lting in electrophysiological alterations in atrial myocytes that may promote AF.

248 tion-PCR to identify partial clones from rat atrial myocytes that share high homology with a member o

249 he results demonstrate directly that, in cat atrial myocytes, the action potential-induced whole-cell

250 However, in atrial myocytes, the effects of shear stress are poorly

251 of the delayed rectifier K+ current in human atrial myocytes, the ultrarapid delayed rectifier K+ cur

252 In adult rat atrial myocytes, three kinetically distinct Ca2+-indepen

253 at beta-adrenoceptors can activate IK,ACh in atrial myocytes through the release of betagamma subunit

254 ectively, but did not alter the responses of atrial myocytes to carbachol.

255 (2+) buffers (EGTA) into voltage-clamped rat atrial myocytes to isolate the fast component of central

256 rated that TGFbeta regulates the response of atrial myocytes to parasympathetic stimulation.

257 We previously reported that attachment of atrial myocytes to the extracellular matrix protein lami

258 ol was significantly prolonged in PMCA1(cko) atrial myocytes under basal conditions, with Ca(2+) over

259 AP and CaT alternans were studied in rabbit atrial myocytes using combined Ca(2+) imaging and electr

260 current for arrhythmia termination in human atrial myocytes using dynamic clamp.

261 g and during Ca(2+) alternans was studied in atrial myocytes using fast confocal microscopy and measu

262 e shear stress-sensitive membrane current in atrial myocytes using the whole-cell patch clamp techniq

263 the central (CT) region of the cell) of cat atrial myocytes using whole-cell voltage-clamp together

264 l alpha1C-unassociated Ca2+-release sites of atrial myocytes, using rapid (240 Hz) two-dimensional co

265 and peripheral sites of voltage-clamped rat atrial myocytes, using rapid 2-dimensional (2-D) confoca

266 currents (Ito, IKur, Ins, and IK1) in human atrial myocytes, using the whole-cell configuration of t

267 activities of three myocyte subpopulations: atrial myocytes, ventricular myocytes, and cells of the

268 fact, for select cardiac cell types such as atrial myocytes, virtually nothing is known regarding en

269 It is concluded that in atrial myocytes voltage-dependent Ca2+ entry triggers Ca

270 hift produced EADs in nine of 17 (53%) human atrial myocytes vs. 0 of 18 from inactivation shift (P <

271 re, the average RMP of embryonic day (ED) 11 atrial myocytes was -22 +/- 2 mV.

272 Native I(f) in nonexpressed atrial myocytes was 7+/-4 pA at -130 mV (n=5), whereas H

273 Basal activity of an AC in isolated atrial myocytes was demonstrated by the observations tha

274 bound gp91phox containing NAD(P)H oxidase in atrial myocytes was the main source of atrial superoxide

275 two-dimensional confocal Ca2+ imaging in rat atrial myocytes, we examine directly the role of I(Ca) o

276 e TATS in excitation-contraction coupling in atrial myocytes, we visualized the TATS (labelled with t

277 Mechanical properties of transgenic atrial myocytes were enhanced to the level of ventricula

278 Atrial myocytes were plated for at least 2 h on uncoated

279 Atrial myocytes were pretreated with vehicle (control) o

280 ency of spark occurrence in the periphery of atrial myocytes where the native alpha1C-RyR complexes a

281 In membrane-permeabilized (saponin-treated) atrial myocytes, where [Ca2+] can be experimentally cont

282 determining membrane potential in embryonic atrial myocytes, where I(K1) is absent.

283 excitation-contraction (E-C) coupling in cat atrial myocytes which lack transverse tubules and contai

284 (2+) wave activity in normal and failing dog atrial myocytes which occurs during the action potential

285 action was also demonstrated in chick embryo atrial myocytes (which do not express endogenous A(3) re

286 s block the Ca(2+)-activated K(+) current in atrial myocytes, which is important for cardiac repolari

287 The data suggest that in atrial myocytes, which lack a t-tubular system, the nj-S

288 In atrial myocytes, which lack t-tubules, ICa inactivation

289 high-density electric mapping, isolation of atrial myocytes, whole-cell patch clamping, in vitro tac

290 Pretreatment of atrial myocytes with 10 nM FSCPX reduced the maximal act

291 imulation of quiescent or electrically paced atrial myocytes with a membrane-permeant InsP3 ester, wh

292 Co-immunostaining of atrial myocytes with antibodies against type II ryanodin

293 Treatment of cultured atrial myocytes with CNTF resulted in a twofold increase

294 type Ca2+ current (beta-ICa,L) of guinea pig atrial myocytes with EC50 values of 2.17 and 0.20 microM

295 Pretreatment of atrial myocytes with FSCPX (50 nM) markedly attenuated t

296 tes lacking t-tubular system and provide the atrial myocytes with functional Ca2+ signaling diversity

297 Treatment of isolated atria or cultured atrial myocytes with recombinant human or avian CNTF res

298 We found two populations of rat atrial myocytes with respect to the ratio of central to

299 Treatment of atrial myocytes with the GSK3beta inhibitor Kenpaullone

300 s activated a large outward current from rat atrial myocytes, with a parallel decrease in action pote