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

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

6 to endoplasmic reticulum (ER) in response to beta-adrenergic stimulation.

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

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

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

10 phai, and functional responses downstream of beta-adrenergic stimulation.

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

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

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

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

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

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

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

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

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

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

21 phosphorylation and cardiac function during beta-adrenergic stimulation.

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

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

24 )1.2 microenvironment but is depleted during beta-adrenergic stimulation.

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

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

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

28 y and Doppler analysis at rest and following beta-adrenergic stimulation.

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

30 ocardial contractility and relaxation during beta-adrenergic stimulation.

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

32 is, twitch force generation, and response to beta-adrenergic stimulation.

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

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

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

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

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

38 ic CAVB rats and worsened when combined with beta-adrenergic stimulation.

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

40 elaxation was significantly decreased during beta-adrenergic stimulation.

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

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

43 phorylation in accelerating relaxation after beta-adrenergic stimulation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 paired excitation-contraction coupling after beta-adrenergic stimulation.

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

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

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

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

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

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

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

79 These effects were reversed by beta-adrenergic stimulation.

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

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

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

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

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

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

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

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

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

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

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

91 Upon cold or beta-adrenergic stimulation, Aifm2 associates with the o

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

93 beta-adrenergic stimulation also induced a broad program

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

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

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

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

98 4F-AG-AMT displayed cardiac-like response to beta-adrenergic stimulation and contractile properties.

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

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

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

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

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

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

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

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

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

108 endent protein kinase II (CaMKII) at Thr(17) beta-Adrenergic stimulation and PKA-dependent phosphoryl

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

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

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

112 yopathies), physiological adaptations (e.g., beta-adrenergic stimulation), and pharmacological interv

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

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

115 lly modulated under basal conditions, during beta-adrenergic stimulation, and in heart failure by mec

116 nnel activity under basal conditions, during beta-adrenergic stimulation, and in heart failure.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Under high glucose and beta-adrenergic stimulation conditions, palmitate can, a

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

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

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

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

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

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

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

153 Acute beta-adrenergic stimulation enhances cardiac contractili

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

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

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

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

158 After beta-adrenergic stimulation, GRK2KO myocytes revealed si

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

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

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

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

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

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

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

166 beta-Adrenergic stimulation in heart leads to increased

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

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

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

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

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

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

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

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

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

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

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

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

179 beta-adrenergic stimulation increases cardiac myosin bin

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

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

182 The fact that beta-adrenergic stimulation increases myocardial oxygen

183 beta-Adrenergic stimulation increases SR content and the

184 beta-Adrenergic stimulation increases stroke volume in m

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

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

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

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

189 Chronic beta-adrenergic stimulation induces myocardial, but not

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

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

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

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

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

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

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

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

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

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

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

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

202 beta-Adrenergic stimulation is the main trigger for card

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

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

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

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

207 The beta-adrenergic stimulation (isoproterenol) and antagoni

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

209 Beta-adrenergic stimulation (isoproterenol, 100 nmol L(-

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

211 beta-Adrenergic stimulation largely overcame the defect

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

213 We found that beta-adrenergic stimulation led to rapidly increased Gal

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

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

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

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

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

219 beta-Adrenergic stimulation of adipose tissue increases

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

221 During beta-adrenergic stimulation of brown adipose tissue (BAT

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

223 beta-Adrenergic stimulation of cardiac muscle activates

224 Here, we investigated whether beta-adrenergic stimulation of cardiomyocytes led to sti

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

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

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

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

229 beta-Adrenergic stimulation of HFpEF myocytes with isopr

230 beta-Adrenergic stimulation of isolated adult cardiomyoc

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

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

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

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

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

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

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

238 bunit-sequestering peptide sharply curtailed beta-adrenergic stimulation of WT Ca2+ channels, identif

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

240 beta-Adrenergic stimulation (often elevated in HF) furth

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

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

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

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

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

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

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

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

249 ls (APs) in ventricular cardiomyocytes under beta-adrenergic stimulation or in disease states remains

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

251 ed ventricular arrhythmias induced by either beta-adrenergic stimulation or programmed ventricular pa

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

253 beta-adrenergic stimulation plays a critical role in acc

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

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

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

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

258 beta-adrenergic stimulation promotes expansion and survi

259 beta-Adrenergic stimulation rapidly activated PKA, which

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

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

262 Beta-adrenergic stimulation resulted in a blunted rise o

263 Thus, beta-adrenergic stimulation results in phosphorylation o

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

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

266 beta-Adrenergic stimulation significantly increased Ptra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 rthermore, L-type Ca(2+) current response to beta-adrenergic stimulation was significantly attenuated

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

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

287 tion and Ca(2+) transients (with and without beta-adrenergic stimulation) were measured at PN90.

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

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

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

291 beta-Adrenergic stimulation with 1.0 micromol/L isoprote

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

293 3, and 6 Hz) in basal conditions and during beta-adrenergic stimulation with isoproterenol (2 nmol/L

294 beta-Adrenergic stimulation with isoproterenol (isoprena

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

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

297 etic db/db mice subjected to stress given by beta-adrenergic stimulation with isoproterenol and high

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

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

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