ライフサイエンスコーパス: beta-adrenergic stimulation

1 activation of protein kinase A (PKA; eg, by beta-adrenergic stimulation).

2 al fibrosis and attenuated responsiveness to beta-adrenergic stimulation).

3 restore myocyte contractility in response to beta adrenergic stimulation.

4 itoring [Ca(2+)](SR) and Ca(2+) waves during beta-adrenergic stimulation.

5 Surprisingly, BAT was not activated during beta-adrenergic stimulation.

6 to achieve localized temporal regulation of beta-adrenergic stimulation.

7 wo steps of adipose lipolysis in response to beta-adrenergic stimulation.

8 ular arrhythmias in young individuals during beta-adrenergic stimulation.

9 phosphorylation and cardiac function during beta-adrenergic stimulation.

10 duced heart rate in response to work load or beta-adrenergic stimulation.

11 evelopment of cardiac hypertrophy induced by beta-adrenergic stimulation.

12 entials; the firing frequency increased with beta-adrenergic stimulation.

13 en species and induction of autophagy during beta-adrenergic stimulation.

14 output changes and is accompanied in vivo by beta-adrenergic stimulation.

15 he L-type Ca2+ channel Cav1.2 in response to beta-adrenergic stimulation.

16 the systolic Ca2+ transient alone and during beta-adrenergic stimulation.

17 ocardial contractility and relaxation during beta-adrenergic stimulation.

18 inetics observed in living myocardium during beta-adrenergic stimulation.

19 n by sildenafil blunts systolic responses to beta-adrenergic stimulation.

20 dels of I(Ks) in the absence and presence of beta-adrenergic stimulation.

21 ced calcium entry, using I(Ks) blockade with beta-adrenergic stimulation.

22 ilar to that of wild type mouse hearts under beta-adrenergic stimulation.

23 horylated by protein kinase A in response to beta-adrenergic stimulation.

24 ions that may be especially important during beta-adrenergic stimulation.

25 elaxation was significantly decreased during beta-adrenergic stimulation.

26 he hypertrophic and antiapoptotic effects of beta-adrenergic stimulation.

27 butes to increased rate of relaxation during beta-adrenergic stimulation.

28 phorylation in accelerating relaxation after beta-adrenergic stimulation.

29 ase channel (ryanodine receptor, RyR) during beta-adrenergic stimulation.

30 ting brown adipocyte function in response to beta-adrenergic stimulation.

31 nt but modifies the hypertrophic response to beta-adrenergic stimulation.

32 nction by phospholamban is a major target of beta-adrenergic stimulation.

33 ergy metabolism, and an abnormal response to beta-adrenergic stimulation.

34 ute to greater contractility in hearts after beta-adrenergic stimulation.

35 I and is essential to the relaxant effect of beta-adrenergic stimulation.

36 r mediating the maximal cardiac responses to beta-adrenergic stimulation.

37 ipates in NO-mediated negative feedback over beta-adrenergic stimulation.

38 , whereas beta-lumicolchicine did not affect beta-adrenergic stimulation.

39 ased by voluntary exercise and by persistent beta-adrenergic stimulation.

40 ulum through PLB phosphorylation mediated by beta-adrenergic stimulation.

41 (SR) through PLB phosphorylation mediated by beta-adrenergic stimulation.

42 inephrine, but not with selective alpha- and beta-adrenergic stimulation.

43 ted, it was no longer sensitive to volume or beta-adrenergic stimulation.

44 ystolic intracellular calcium in response to beta-adrenergic stimulation.

45 ine but preserved NO activity in response to beta-adrenergic stimulation.

46 markedly blunted the contractile response to beta-adrenergic stimulation.

47 lowed relaxation, and depressed responses to beta-adrenergic stimulation.

48 ude of contraction) but were unresponsive to beta-adrenergic stimulation.

49 e explained by changes in the sensitivity to beta-adrenergic stimulation.

50 ng the contractile responses of the heart to beta-adrenergic stimulation.

51 culum which is phosphorylated in response to beta-adrenergic stimulation.

52 n cardiac contractile parameters and loss of beta-adrenergic stimulation.

53 creased cardiac contractility in response to beta-adrenergic stimulation.

54 ythmias in structurally normal hearts during beta-adrenergic stimulation.

55 contribute to the net stimulatory effect of beta-adrenergic stimulation.

56 refractory for several minutes from further beta-adrenergic stimulation.

57 Ms restores a positive inotropic response to beta-adrenergic stimulation.

58 role in modulating troponin function during beta-adrenergic stimulation.

59 r cTnI (KC-I) or contractile kinetics during beta-adrenergic stimulation.

60 phorylation by protein kinase A (PKA) during beta-adrenergic stimulation.

61 chronotropic but null inotropic responses to beta-adrenergic stimulation.

62 of cTn by phosphorylation of S23/S24 during beta-adrenergic stimulation.

63 ilin-2 and lethal arrhythmias in response to beta-adrenergic stimulation.

64 These effects were reversed by beta-adrenergic stimulation.

65 ance early phase diastolic relaxation during beta-adrenergic stimulation.

66 omoted early-after-depolarisations following beta-adrenergic stimulation.

67 Ca(2+) release in cardiac myocytes evoked by beta-adrenergic stimulation.

68 n adipocyte differentiation and activated by beta-adrenergic stimulation.

69 use of increased intracellular Ca(2+) during beta-adrenergic stimulation.

70 ncy response and the contractile response to beta-adrenergic stimulation.

71 n of spark-mediated J(leak) increases due to beta-adrenergic stimulation.

72 of arrhythmias in human atrial strips during beta-adrenergic stimulation.

73 x sensitized PKA phosphorylation of KCNQ1 to beta-adrenergic stimulation.

74 amatically delayed their decay after a brief beta-adrenergic stimulation.

75 t WT and mutant Kv11.1 channels responded to beta-adrenergic stimulation.

76 nst pro-arrhythmogenic Ca(2+) release during beta-adrenergic stimulation.

77 duction in channel activation in response to beta-adrenergic stimulation.

78 idation and opposes the metabolic effects of beta-adrenergic stimulation.

79 During beta-adrenergic stimulation (100 nM isoproterenol), only

80 rrhythmia-prone EBZ tissue to desensitize to beta-adrenergic stimulation 24 hours after CAL.

81 decrease in spark-to-spark delays seen with beta-adrenergic stimulation; (5) inhibiting either PKA o

82 decrease in spark-to-spark delays seen with beta-adrenergic stimulation; (5) inhibiting either PKA o

83 ically paced myocytes, both with and without beta-adrenergic stimulation (70 nM isoproterenol (isopre

84 monary cAMP and AFC were also observed after beta-adrenergic stimulation, a pathway known to promote

85 Inhibition of GSK3beta by beta-adrenergic stimulation abrogates GSK3beta-induced n

86 ity and impaired chronotropic response under beta-adrenergic stimulation, accompanied by the appearan

87 ed a significant increase in the response to beta-adrenergic stimulation after LVAD (developed tensio

88 e PTX treatment increases the sensitivity to beta-adrenergic stimulation alone and that this could ac

89 beta-adrenergic stimulation also induced a broad program

90 ined in both the absence and the presence of beta-adrenergic stimulation although the beta-agonist ac

91 calcium channels become phosphorylated after beta-adrenergic stimulation, although this does not lead

92 ve inotropic response of the murine heart to beta-adrenergic stimulation, an effect that is highly de

93 association between ion channel response to beta-adrenergic stimulation and clinical response to bet

94 4F-AG-AMT displayed cardiac-like response to beta-adrenergic stimulation and contractile properties.

95 of contraction are increased in response to beta-adrenergic stimulation and high-frequency electrica

96 and amplitude of cardiac contraction during beta-adrenergic stimulation and increased stimulus frequ

97 such modulation enhances rather than blunts beta-adrenergic stimulation and is accompanied by increa

98 ation of L-type Ca2+ currents in response to beta-adrenergic stimulation and local increases in cAMP.

99 his blunts the local contractile response to beta-adrenergic stimulation and may serve to protect aga

100 and this process is dynamically regulated by beta-adrenergic stimulation and phosphorylation of phosp

101 n hypertrophic hearts in response to chronic beta-adrenergic stimulation and PKA activation.

102 n hypertrophic hearts in response to chronic beta-adrenergic stimulation and PKA activation.

103 periments were performed to test the role of beta-adrenergic stimulation and PKA phosphorylation of S

104 iminished hypertrophy in response to chronic beta-adrenergic stimulation and pressure overload.

105 e NO/nitrates is independent and additive to beta-adrenergic stimulation and stimulates CGRP release.

106 interactive effect between oil-exposure and beta-adrenergic stimulation and suggests if animals achi

107 n of cGMP in the heart can potently modulate beta-adrenergic stimulation, and alterations in enzyme l

108 This regulation is coupled to beta-adrenergic stimulation, and dysfunction has been as

109 fractional shortening and responsiveness to beta-adrenergic stimulation, and it limited development

110 ncement of cardiac function that occurs upon beta-adrenergic stimulation, and mutations in MyBP-C cau

111 pment and relaxation as a result of enhanced beta-adrenergic stimulation, and reduced MyBP-C phosphor

112 y cytokine expression through alpha- but not beta-adrenergic stimulation, and suggest that such alpha

113 We show that Jhdm2a expression is induced by beta-adrenergic stimulation, and that Jhdm2a directly re

114 loss of inotropic reserve, uncovered during beta-adrenergic stimulation, and the presence of cardiac

115 e (Ca(2+) wave latency) was prolonged during beta-adrenergic stimulation, and was highly dependent on

116 tion, and apoptosis in response to sustained beta-adrenergic stimulation; and (3) the beneficial effe

117 rdiac function and the inotropic response to beta-adrenergic stimulation are impaired in sepsis.

118 insufficient to regulate respiration during beta-adrenergic stimulation, arguing against intracrine

119 arts exhibit positive inotropic responses to beta-adrenergic stimulation as a consequence of protein

120 Chronic beta-adrenergic stimulation, as occurs in patients with

121 lates action potential duration (APD) during beta-adrenergic stimulation at different heart rates are

122 sights into arrhythmogenic mechanisms during beta-adrenergic stimulation besides triggered activity a

123 To achieve beta-adrenergic stimulation (beta effect), cells were su

124 uggests responsiveness (increase in rate) to beta-adrenergic stimulation (betaAS), as observed experi

125 beta-adrenergic stimulation breaks the delicate Ca(2+) e

126 ontractility and the contractile response to beta-adrenergic stimulation by a NO-cGMP-mediated decrea

127 ed that the activation of glycolysis through beta-adrenergic stimulation by endogenous catecholamines

128 v11.1 and T421M-Kv11.1 channels responded to beta-adrenergic stimulation by increasing I(Kv11.1).

129 herefore conclude that systemic nonselective beta-adrenergic stimulation by ISO at concentrations tha

130 Responses to beta-adrenergic stimulation (by isoproterenol) were grea

131 AMP (cAMP) concentrations, a known effect of beta-adrenergic stimulation, by addition of dibutyryl cA

132 Under beta-adrenergic stimulation, Ca(2+) transient amplitude,

133 Under beta-adrenergic stimulation, [Ca2+]m decay was approxima

134 by a Ca-regulated kinase is necessary before beta-adrenergic stimulation can produce additional phosp

135 on of TSC2 gene activity in combination with beta-adrenergic stimulation can reactivate the cell cycl

136 During beta-adrenergic stimulation, cardiac troponin I (cTnI) i

137 Our results demonstrate that, in response to beta-adrenergic stimulation, cardiomyocyte function and

138 vate alpha 1-receptors while maintaining the beta-adrenergic stimulation, cells were superfused with

139 However, with increased heart rate or beta-adrenergic stimulation, cTnIS200D mice had less enh

140 show a blunted cardiac inotropic response to beta-adrenergic stimulation despite normal cardiac contr

141 fter induction of apoptotic pathway by using beta-adrenergic stimulation, displayed a similar pattern

142 On pathological pressure overload and beta-adrenergic stimulation, DKO mice are protected agai

143 In PLM knockout (PLM-KO) mice in which beta-adrenergic stimulation does not activate NKA, [Na](

144 is phosphorylated at Ser16 and Thr17 during beta-adrenergic stimulation (eg, isoproterenol).

145 We found that beta-adrenergic stimulation elicits exocytosis of large

146 beta-adrenergic stimulation enhanced ensemble-averaged c

147 Acute beta-adrenergic stimulation enhances cardiac contractili

148 We conclude that beta-adrenergic stimulation enhances the Frank-Starling

149 We conclude that beta-adrenergic stimulation enhances the gain of the CIC

150 response to IL-1beta via induction of iNOS; beta-adrenergic stimulation enhances the IL-1beta effect

151 Cold exposure or beta-adrenergic stimulation favors the active thermogeni

152 After beta-adrenergic stimulation, GRK2KO myocytes revealed si

153 ac function under stress; however, sustained beta-adrenergic stimulation has been implicated in patho

154 ein-C (MyBP-C), are phosphorylated following beta-adrenergic stimulation; however, their relative con

155 DAC9 show a hypertrophic response to chronic beta-adrenergic stimulation identical to that of wild-ty

156 But when coupled with beta-adrenergic stimulation in a whole-cell model, the K

157 tudy was to evaluate the diagnostic value of beta-adrenergic stimulation in ARVC.

158 creased by approximately 12% within 3 min of beta-adrenergic stimulation in beating cardiac myocytes.

159 amplitude of the Ca2+ transient produced by beta-adrenergic stimulation in cardiac muscle is due to

160 beta-Adrenergic stimulation in heart leads to increased

161 inhibits the positive inotropic response to beta-adrenergic stimulation in humans with left ventricu

162 ort improved force generation in response to beta-adrenergic stimulation in isolated LV (increase in

163 lation of phospholamban and troponin I after beta-adrenergic stimulation in isolated myocytes.

164 al contraction and the inotropic response to beta-adrenergic stimulation in murine ventricular myocyt

165 tentiates the positive inotropic response to beta-adrenergic stimulation in patients with symptomatic

166 e that activation of the Ca-ATPase following beta-adrenergic stimulation in the heart only occurs abo

167 xtent of contractility and relaxation during beta-adrenergic stimulation in the intact animal remain

168 y was undertaken to test the hypothesis that beta-adrenergic stimulation in the setting of membrane d

169 tein accounted for the ICaL insensitivity to beta-adrenergic stimulation in VEDS cardiomyocytes.

170 rophy and enhanced cardiac responsiveness to beta-adrenergic stimulation in vivo.

171 prevents phosphorylation of serine 1928 upon beta-adrenergic stimulation in vivo.

172 tive amplitude-frequency relationship and in beta-adrenergic stimulation, including decreasing and in

173 beta-adrenergic stimulation increases cardiac myosin bin

174 In cardiac muscle, beta-adrenergic stimulation increases contractile force

175 beta-adrenergic stimulation increases I(Ks) and results

176 The fact that beta-adrenergic stimulation increases myocardial oxygen

177 beta-Adrenergic stimulation increases SR content and the

178 beta-Adrenergic stimulation increases stroke volume in m

179 s show increased TDR compared with LQT1, and beta-adrenergic stimulation increases TDR in both models

180 These data show that acute beta-adrenergic stimulation increases the [Ca(2+)](SR) t

181 ll, the results presented here indicate that beta-adrenergic stimulation increases the spark-dependen

182 ted lusitropic response of cardiac muscle to beta-adrenergic stimulation indicate a novel pathogenic

183 Chronic beta-adrenergic stimulation induces myocardial, but not

184 In the heart, beta-adrenergic stimulation induces protein kinase A pho

185 Our data suggest that beta-adrenergic stimulation induces TdP by increasing tr

186 mouse ventricular myocytes by examining how beta-adrenergic stimulation influenced sequences of Ca(2

187 mouse ventricular myocytes by examining how beta-adrenergic stimulation influenced sequences of Ca2+

188 important role in sinus acceleration during beta-adrenergic stimulation, interacting synergistically

189 e hypothesis that sinus rate acceleration by beta-adrenergic stimulation involves synergistic interac

190 Because beta-adrenergic stimulation is a frequent trigger of arr

191 Our study shows that increased beta-adrenergic stimulation is a potentially highly sign

192 Contractile reserve during submaximal beta-adrenergic stimulation is attenuated in patients an

193 e increased incidence of Ca(2+) waves during beta-adrenergic stimulation is due to an alteration in t

194 ggest that the increase in arrhythmias after beta-adrenergic stimulation is independent of enhanced E

195 The increase in Ser-845 phosphorylation upon beta-adrenergic stimulation is much more severely impair

196 beta-Adrenergic stimulation is the main trigger for card

197 An important target of beta-adrenergic stimulation is the sarcolemmal L-type Ca

198 lation in the positive inotropic response to beta-adrenergic stimulation is unclear.

199 s the endogenous theta-rhythm and depends on beta-adrenergic stimulation, is only modestly affected i

200 Under current clamp, beta-adrenergic stimulation (isoprenaline, 30 nm) increa

201 tivation (caffeine and 4-chloro-m-cresol) or beta-adrenergic stimulation (isoproterenol).

202 s if animals achieve very large increases in beta-adrenergic stimulation it could play a compensatory

203 beta-Adrenergic stimulation largely overcame the defect

204 s shown that BVR is increased during intense beta-adrenergic stimulation, leading to SCR.

205 d cardiomyocytes exhibited responsiveness to beta-adrenergic stimulation manifest by an increase in s

206 CaMKII and PKA activities during beta-adrenergic stimulation may synergistically facilita

207 equency response; (4) inotropic responses to beta-adrenergic stimulation mediated via canonical beta1

208 s in myocardial excitability are mediated by beta-adrenergic stimulation of a cAMP-sensitive K(+) cur

209 These data demonstrate that beta-adrenergic stimulation of a PGC-1alpha/ERRalpha/VEG

210 In summary, the beta-2 receptor mediates beta-adrenergic stimulation of alveolar epithelial sodiu

211 Interestingly, beta-adrenergic stimulation of both Rap1 and ERKs, but n

212 e RyR/FKBP12.6 association, suggesting minor beta-adrenergic stimulation of Ca2+ release through this

213 beta-Adrenergic stimulation of cardiac muscle activates

214 vention of C-terminal cleavage did not alter beta-adrenergic stimulation of CaV1.2 in the heart.

215 nsus PKA phosphorylation sites in alpha1C in beta-adrenergic stimulation of CaV1.2, and show that pho

216 ytic cleavage of alpha1C is not required for beta-adrenergic stimulation of CaV1.2.

217 motif abolishes insulin counterregulation of beta-adrenergic stimulation of cyclic AMP accumulation a

218 of CaV1.2 channels in cardiac myocytes, and beta-adrenergic stimulation of L-type Ca2+ currents in t

219 uation by muscarinic cholinergic agonists of beta-adrenergic stimulation of L-type calcium current an

220 y adults demonstrate reduced, not increased, beta-adrenergic stimulation of metabolic rate because of

221 Conversely, beta-adrenergic stimulation of PGC-1alpha(-/-) cells res

222 beta-Adrenergic stimulation of SR Ca2+ uptake in cells f

223 Furthermore, the ability of PVN to inhibit beta-adrenergic stimulation of the Ca(2+) current was an

224 Beta-adrenergic stimulation of the heart results in an e

225 During beta-adrenergic stimulation of the heart, there is a dec

226 We aimed to investigate whether simultaneous beta-adrenergic stimulation offsets this balance in youn

227 ) and quantitatively examined the effects of beta-adrenergic stimulation on channel kinetics.

228 etion (NRG-1+/-) and examined the effects of beta-adrenergic stimulation on contractility in the pres

229 kedly with advancing age, but the effects of beta-adrenergic stimulation on filling, and its major de

230 l systems, we studied the effects of chronic beta-adrenergic stimulation on the myocardial and system

231 The effect of beta-adrenergic stimulation on the relationship between

232 ovel determinants of the inotropic effect of beta-adrenergic stimulation on the ventricular heart mus

233 Ca2+ channel (LCC) phosphorylation, such as beta-adrenergic stimulation or an increased expression o

234 Conversely, chronic beta-adrenergic stimulation or expression of an activate

235 tor of increased contractility observed with beta-adrenergic stimulation or increased pacing because

236 greatly enhanced contraction in response to beta-adrenergic stimulation (percent increase in contrac

237 beta-adrenergic stimulation plays a critical role in acc

238 -dependent protein kinase II (CaMKII) during beta-adrenergic stimulation prevented the decrease in sp

239 -dependent protein kinase II (CaMKII) during beta-adrenergic stimulation prevented the decrease in sp

240 open probability alone or in the presence of beta-adrenergic stimulation produces diastolic Ca releas

241 Short-term beta-adrenergic stimulation promotes contractility in re

242 beta-adrenergic stimulation promotes expansion and survi

243 beta-Adrenergic stimulation rapidly activated PKA, which

244 S1928 displaces the beta2AR from Cav1.2 upon beta-adrenergic stimulation rendering Cav1.2 refractory

245 n of PKA substrates, elicited in response to beta-adrenergic stimulation, require spatially confined

246 Beta-adrenergic stimulation resulted in a blunted rise o

247 Thus, beta-adrenergic stimulation results in phosphorylation o

248 In the presence of beta-adrenergic stimulation, RyR-mediated Ca leak produc

249 Additionally, with beta-adrenergic stimulation, scavenging of mitochondrial

250 beta-Adrenergic stimulation significantly increased Ptra

251 In voltage clamp experiments, beta-adrenergic stimulation still increased SR Ca2+ cont

252 contractions and responding more strongly to beta-adrenergic stimulation than wild-type cells.

253 roteins in the heart to be phosphorylated by beta-adrenergic stimulation, the functional impact of ph

254 on, demonstrating a defect in the ability of beta-adrenergic stimulation to regulate sarcoplasmic ret

255 plus phentolamine (10 micromol/L, selective beta-adrenergic stimulation) to the perfusate.

256 ed sensitivity to frequency potentiation and beta-adrenergic stimulation, two major physiological mec

257 on represents a key signaling mechanism upon beta-adrenergic stimulation under stress.

258 Pharmacological and physiological beta-adrenergic stimulation upregulates FGF10 levels and

259 epolarisations or abnormal automaticity with beta-adrenergic-stimulation, using the dynamic-clamp tec

260 The acute insulin secretory response to beta-adrenergic stimulation was also profoundly suppress

261 Cardiac chronotropic responsiveness to beta-adrenergic stimulation was assessed in vitro using

262 pressure development observed in response to beta-adrenergic stimulation was attenuated in TG(S282A)

263 in aP2-/- mice, the plasma FFA profile after beta-adrenergic stimulation was determined.

264 ibitory G-protein (Galpha(i)) suppression of beta-adrenergic stimulation was greater in DHF and rever

265 ulation of Krebs cycle dehydrogenases during beta-adrenergic stimulation was hampered in Mfn2-KO but

266 ronic AF patients, their response to maximal beta-adrenergic stimulation was not impaired.

267 However, cardiac reserve to work load and beta-adrenergic stimulation was reduced.

268 of LL absorption postnatally, and that while beta-adrenergic stimulation was the sole source of endog

269 tolic pressure and the effects of alpha- and beta-adrenergic stimulation were examined in both models

270 erturbations or intrinsic signaling, such as beta-adrenergic stimulation, which regulate cardiac calc

271 t relevant source of intracellular NO during beta-adrenergic stimulation, while no evidence for a mit

272 Increased SERCA activity (beta-adrenergic stimulation with 1 muM isoproterenol (is

273 beta-Adrenergic stimulation with 1.0 micromol/L isoprote

274 Time-averaged [Ca(2+) ]i was increased by beta-adrenergic stimulation with isoprenaline and increa

275 3, and 6 Hz) in basal conditions and during beta-adrenergic stimulation with isoproterenol (2 nmol/L

276 beta-Adrenergic stimulation with isoproterenol (isoprena

277 ences measured under control conditions: (1) beta-adrenergic stimulation with isoproterenol (isoprena

278 ences measured under control conditions: (1) beta-adrenergic stimulation with isoproterenol (isoprena

279 not alter the intracellular Ca2+ response to beta-adrenergic stimulation with isoproterenol but atten

280 We hypothesized that blockade of beta-adrenergic stimulation with propranolol would decre

281 in cardiac functional reserve in response to beta-adrenergic stimulation without significant alterati