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

1 antagonist-GPCR complex of iodopindolol and beta-adrenergic receptor.

2 coupled receptor desensitization, especially beta-adrenergic receptors.

3 eceptors, whereas activation was mediated by beta-adrenergic receptors.

4 nt-binding protein pathway downstream of the beta-adrenergic receptors.

5 e of catecholamines and activation of muscle beta-adrenergic receptors.

6 o binding of agonists to the prostacyclin or beta-adrenergic receptors.

7 al tone and for their linkage to vasodilator beta-adrenergic receptors.

8 ents in genetically manipulated mice lacking beta-adrenergic receptors.

9 ramatically enhanced by acute stimulation of beta-adrenergic receptors.

10 e on I(Na), I(Kur), I(CaL), I(CaT), I(f) and beta-adrenergic receptors.

11 are comorbid, which involves the activity of beta-adrenergic receptors.

12 rmacological inhibition of muscarinic and/or beta-adrenergic receptors.

13 e Ras, and is induced upon the activation of beta-adrenergic receptors.

14 trosylation after agonist stimulation of the beta-adrenergic receptor, a prototypical GPCR, dissociat

15 hway and intra-BLA or systemic antagonism of beta-adrenergic receptors abolished both long-term pain-

16 phenotype had elevated serum titers of anti-beta-adrenergic receptor Abs, as well as increased prote

17 Here we show that beta-adrenergic receptors activate eight Galphas mutant

18 to confer this cytoprotective consequence of beta adrenergic receptor activation in this cell model.

19 We also show that beta-adrenergic receptor activation by catecholamine of

20 act heart protects against cardiotoxicity of beta-adrenergic receptor activation by isoproterenol (IS

21 beta-Adrenergic receptor activation increases the Ca(2)(

22 In the failing heart, persistent beta-adrenergic receptor activation is thought to induce

23 ough voltage-dependent calcium channels upon beta-adrenergic receptor activation.

24 mulated by angiotensin II, but not following beta-adrenergic receptor activation.

25 unction of the intact heart independently of beta-adrenergic receptor activation.

26 those encoding lactate transporter MCT2 and beta-adrenergic receptor ADRB2, are strongly (~20-fold)

27 ances in glucose homeostasis with associated beta adrenergic receptor (ADRbeta) desensitization.

28 n/Hsp27 complex in response to the selective beta adrenergic receptor agonist isoproterenol, was subs

29 Administration of L-arginine and a beta-adrenergic receptor agonist (CL316, 243, respective

30 sed to cold temperatures or treated with the beta-adrenergic receptor agonist CL316,243 and that its

31 following intra-LS injections of either the beta-adrenergic receptor agonist isoproterenol (10 mug o

32 during periodic pacing in the presence of a beta-adrenergic receptor agonist isoproterenol, was sign

33 reated some cells with Compound 49b, a novel beta-adrenergic receptor agonist we have reported previo

34 ulation can be triggered by isoproterenol (a beta-adrenergic receptor agonist) treatment.

35 g treatment with 50 nM Compound 49b, a novel beta-adrenergic receptor agonist.

36 ve agonist, or isoprenaline, a non-selective beta-adrenergic receptor agonist.

37 These studies demonstrate that beta-adrenergic receptor agonists in vitro can restore t

38 also sensitizes the channel to activation by beta-adrenergic receptor agonists.

39 was threefold greater than that elicited by beta-adrenergic receptor agonists.

40 ort recent evidence indicating that blocking beta-adrenergic receptors alone shortly after trauma may

41 In heart failure, common genetic variants of beta-adrenergic receptors, alpha-adrenergic receptors, a

42 to signal transduction networks that include beta-adrenergic receptors, alpha-amino-3-hydroxyl-5-meth

43 nd in most mammalian cells, the mechanism of beta- adrenergic receptor and AC compartmentalization ma

44 inephrine, a catecholamine that binds to the beta-adrenergic receptor and activates the cAMP-PKA-depe

45 art failure work by targeting GPCRs, such as beta-adrenergic receptor and angiotensin II receptor ant

46 beta-Adrenergic receptor and inotropic response were dec

47 l activity and mediates up-regulation by the beta-adrenergic receptor and PKA bound to A-kinase ancho

48 lamine biosynthesis and release, stimulating beta-adrenergic receptors and activating cAMP signaling

49 rdiac contractile signaling/function through beta-adrenergic receptors and metabolism through the ins

50 It is known that beta-adrenergic receptors and NA can boost LTP maintenan

51 ential value of biased ligands targeting the beta-adrenergic receptors and nicotinic acid receptor GP

52 indicate that both proteins are regulated by beta-adrenergic receptors and respond antagonistically.

53 ase showed no recovery, while phospholamban, beta-adrenergic receptor, and the inotropic response ful

54 beta-adrenergic receptor antagonism after experimental s

55 Overall, beta-adrenergic receptor antagonism produced a dysfuncti

56 and absence of a alpha2-agonist (clonidine), beta-adrenergic receptor antagonist (propranolol), and b

57 Here, we asked whether a beta-adrenergic receptor antagonist might interfere with

58 ug or 30 mug) or vehicle (Experiment 1), the beta-adrenergic receptor antagonist propranolol (2 mug)

59 We probed the effects of the beta-adrenergic receptor antagonist propranolol (40 mg)

60 We find that administration of the beta-adrenergic receptor antagonist propranolol before m

61 Healthy participants were administered the beta-adrenergic receptor antagonist propranolol or a pla

62 The beta-adrenergic receptor antagonist propranolol, adminis

63 Propranolol is a nonselective beta-adrenergic receptor antagonist that is efficacious

64 herapies is also enhanced by administering a beta-adrenergic receptor antagonist to mice housed at 22

65 e expression, but pre-exposure to timolol, a beta-adrenergic receptor antagonist, delayed this effect

66 r antagonist, or propranolol, a nonselective beta-adrenergic receptor antagonist, delivered by osmoti

67 macrophages were prevented by propranolol, a beta-adrenergic receptor antagonist.

68 etimes increased by treatment with IL-4 or a beta-adrenergic receptor antagonist.

69 For many years, beta-adrenergic receptor antagonists (beta-blockers or b

70 hese responses can be inhibited by alpha and beta-adrenergic receptor antagonists implying a bacteria

71 Systemic application of beta-adrenergic receptor antagonists may have detrimenta

72 Orthosteric beta-adrenergic receptor antagonists, known as beta-bloc

73 Despite widespread usage of beta-adrenergic receptor (AR) agonists and antagonists i

74 Beta-adrenergic receptor (AR) antagonists are frequently

75 beta-Adrenergic receptor (AR) blockers provide substanti

76 ation and determine the roles of alpha1- and beta-adrenergic receptors (AR) in the loss-of-interest i

77 and other organ thermogenesis occurs through beta-adrenergic receptors (AR), and considerable effort

78 To determine whether beta-adrenergic receptors are involved in the modulation

79 ense noradrenergic innervation and expresses beta adrenergic receptors (ARs).

80 Agonist-triggered downregulation of beta-adrenergic receptors (ARs) constitutes vital negati

81 Retromer-associated endosomes contain beta-adrenergic receptors as well as ionotropic glutamat

82 ious work has demonstrated that a functional beta-adrenergic receptor autocrine/paracrine network exi

83 Postsynaptic function, beta-adrenergic receptor (BAR) density (B'(max)), was me

84 e glucose counterregulation via specific VMH beta-adrenergic receptors (BAR).

85 Propranolol (beta-adrenergic receptor (beta-Ad) antagonist) enhanced

86 nd vasorelaxation is enhanced in response to beta-adrenergic receptor (beta-AdR) agonists in vitro.

87 beta-Adrenergic receptor (beta-AR) activation can provok

88 cently, we and others have demonstrated that beta-adrenergic receptor (beta-AR) activation is necessa

89 trieval and reconsolidation are dependent on beta-adrenergic receptor (beta-AR) activation.

90 ssion is markedly induced in the heart after beta-adrenergic receptor (beta-AR) activation.

91 beta-Adrenergic receptor (beta-AR) agonists are the most

92 beta-Adrenergic receptor (beta-AR) blockers administered

93 Chronic beta-adrenergic receptor (beta-AR) overstimulation, a ha

94 old stimuli and the subsequent activation of beta-adrenergic receptor (beta-AR) potently stimulate ad

95 teins and their receptor integrins influence beta-adrenergic receptor (beta-AR) responses in vitro, w

96 e, a condition associated with diminution of beta-adrenergic receptor (beta-AR) responsiveness.

97 g therapies to improve heart function target beta-adrenergic receptor (beta-AR) signaling and Ca(2+)

98 r kinase-2 (GRK2) is a critical regulator of beta-adrenergic receptor (beta-AR) signaling and cardiac

99 We used beta-adrenergic receptor (beta-AR) signaling as a protot

100 (HF) and determined PDE2-mediated effects on beta-adrenergic receptor (beta-AR) signaling in healthy

101 beta-Adrenergic receptor (beta-AR) signaling is a pathwa

102 beta-adrenergic receptor (beta-AR) signaling was markedl

103 While beta-adrenergic receptor (beta-AR) stimulation ensures a

104 While beta-adrenergic receptor (beta-AR) stimulation leads to

105 Intracellular Ca(2+) ([Ca(2+) ]i ) and beta-adrenergic receptor (beta-AR) stimulation modulate

106 effect of SIT on the thermogenic response to beta-adrenergic receptor (beta-AR) stimulation, an impor

107 volved in cardiac dysfunction during chronic beta-adrenergic receptor (beta-AR) stimulation.

108 ulates myocardial calcium transients through beta-adrenergic receptor (beta-AR)-mediated phosphorylat

109 ore prevalent mechanism and hypothesize that beta-adrenergic receptor (beta-AR)-mediated regulation o

110 It causes pathologic desensitization of beta-adrenergic receptors (beta-AR), facilitated predomi

111 co-activation of G(q)-coupled receptors and beta-adrenergic receptors (beta-AR), leading to cardiac

112 that stimulates contractility by activating beta-adrenergic receptors (beta-AR).

113 n of sympathetic nerve fibers, expression of beta-adrenergic receptors (beta-ARs) and remodeling para

114 Activation of beta-adrenergic receptors (beta-ARs) can induce a functi

115 receptor kinase (GRK)2 to agonist-stimulated beta-adrenergic receptors (beta-ARs) in HF, leading to c

116 beta-Adrenergic receptors (beta-ARs) promote brown adipo

117 We have shown that beta-adrenergic receptors (beta-ARs), which are activate

118 nnels can be modulated through activation of beta-adrenergic receptors (beta-ARs), which leads to an

119 also associated with enhanced stimulation of beta-adrenergic receptors (beta-ARs).

120 Activation of the beta adrenergic receptor (betaAR) induces a tightly cont

121 We examined the effect of beta-adrenergic receptor (betaAR) activation and cAMP-el

122 mechanisms underlying synaptic responses to beta-adrenergic receptor (betaAR) activation remain poor

123 action potential duration (APD), mediated by beta-adrenergic receptor (betaAR) activation, requires a

124 ermore, these responses were mimicked by the beta-adrenergic receptor (betaAR) agonist isoproterenol,

125 yclic nucleotide-gated ion channel (HCN4) by beta-adrenergic receptor (betaAR) agonist stimulation.

126 fter stimulation with isoproterenol (ISO), a beta-adrenergic receptor (betaAR) agonist.

127 Beta-adrenergic receptor (betaAR) blockade is a standard

128 mor necrosis factor-alpha (TNFalpha) induces beta-adrenergic receptor (betaAR) desensitization, but m

129 udies have demonstrated associations between beta-adrenergic receptor (betaAR) polymorphisms and left

130 se (GRK)2 is a critical regulator of cardiac beta-adrenergic receptor (betaAR) signaling and cardiac

131 rdium appears to contribute to dysfunctional beta-adrenergic receptor (betaAR) signaling and cardiac

132 pharmacological and genetic manipulation of beta-adrenergic receptor (betaAR) signaling in osteoblas

133 A (PKA) are the most widely studied steps in beta-adrenergic receptor (betaAR) signaling in the heart

134 at least in part by normalization of cardiac beta-adrenergic receptor (betaAR) signaling.

135 We found that beta-adrenergic receptor (betaAR) stimulation induces up

136 psilon that plays a critical role in maximal beta-adrenergic receptor (betaAR) stimulation of Ca2+-in

137 a pharmacogenetic study for two predominant beta-adrenergic receptor (betaAR) subtypes expressed in

138 erent lines of evidence, we propose that the beta-adrenergic receptor (betaAR), cAMP and the transcri

139 Activation of the beta-adrenergic receptor (betaAR)/cAMP/protein kinase A

140 nhibits protein phosphatase 2A (PP2A) at the beta-adrenergic receptor (betaAR, a GPCR) complex alteri

141 Beta adrenergic receptors (betaARs) are G-protein-couple

142 tores by hydrolysis of triglycerides through beta-adrenergic receptor (betaARs) and protein kinase A

143 a SUMOylation-deficient mutant of Cav-3 with beta-adrenergic receptors (betaARs) alters the expressio

144 beta-adrenergic receptors (betaARs) are critical regulat

145 beta-adrenergic receptors (betaARs) are G-protein-couple

146 In heart failure, the beta-adrenergic receptors (betaARs) become desensitized

147 Activation of beta-adrenergic receptors (betaARs) enhances both the in

148 It is unclear whether cAMP generated by beta-adrenergic receptors (betaARs) is required for PF-P

149 Stimulation of beta-adrenergic receptors (betaARs) provides the most ef

150 epinephrine, a neuromodulator that activates beta-adrenergic receptors (betaARs), facilitates learnin

151 that norepinephrine, through its actions on beta-adrenergic receptors (betaARs), modulates aversive

152 riety of signals such as those stimulated by beta-adrenergic receptors (betaARs).

153 oubled through the neuromodulatory action of beta-adrenergic receptors (betaARs).

154 n to regulate immune system function through beta-adrenergic receptors (betaARs); however, their role

155 ndent dilation) before and after local alpha+beta adrenergic receptor blockade (phentolamine and prop

156 n other cardiovascular diseases treated with beta-adrenergic receptor blockade (BB).

157 beta-adrenergic receptor blockade after ACS is a measure

158 restoration of KORs in the LC together with beta-adrenergic receptor blockade did not potentiate KOR

159 Traditional medical therapies, such as beta-adrenergic receptor blockade, are used to slow path

160 We hypothesized that beta-adrenergic receptor blocker (beta-blocker) and angi

161 yields of optically pure triazole-containing beta-adrenergic receptor blocker analogues with potentia

162 Importantly, beta-adrenergic receptor blocker therapy has been also s

163 network in the context of heart failure and beta-adrenergic receptor blocker therapy, where multiple

164 Propranolol, a nonselective beta-adrenergic receptor blocker, was reported to protec

165 beta-Adrenergic receptor blockers (beta-blockers) are co

166 ssary to characterize the appropriate use of beta-adrenergic receptor blockers (beta-blockers) in the

167 drugs that target neurohormonal activation: beta-adrenergic receptor blockers (beta-blockers), ACE (

168 nt relies on pharmacological therapy, mostly beta-adrenergic receptor blockers (specifically, propran

169 th in patients with heart failure, for which beta-adrenergic receptor blockers are a mainstay therapy

170 In contrast, beta-adrenergic receptor blockers improved cardiac funct

171 The stimulation of beta-adrenergic receptors by isoproterenol (ISO) resulte

172 response hormone norepinephrine to stimulate beta-adrenergic receptors, cAMP production, and protein

173 se muscle contractility by activation of the beta-adrenergic receptor/cAMP-dependent protein kinase p

174 Inhibition of the beta-adrenergic receptor/cAMP/PKA axis protected against

175 revailing dogma holds that activation of the beta-adrenergic receptor/cAMP/protein kinase A signallin

176 Catecholamines bind to beta-adrenergic receptors, causing cAMP generation and a

177 o restored by stimulating A(2A) adenosine or beta-adrenergic receptors, consistent with G(s)-protein

178 gs offer additional mechanistic insights how beta-adrenergic receptor-controlled PKA activities enhan

179 heart, adrenergic stimulation activates the beta-adrenergic receptors coupled to the heterotrimeric

180 of the T-type Ca(2+) current is initiated by beta-adrenergic receptors, cyclic AMP and cyclic AMP-dep

181 This change was initiated by beta-adrenergic receptors, cyclic AMP and protein kinase

182 duced myocardial contractility, decreases in beta-adrenergic receptor density and increases in Galpha

183 and ryanodine receptor proteins, as well as beta-adrenergic receptor density in nonfailing, hypertro

184 isal and promoted anxiety-like behavior in a beta-adrenergic receptor-dependent manner.

185 ulated by acute treadmill exercise through a beta-adrenergic receptor-dependent mechanism.

186 ercise increases SKM D2 expression through a beta-adrenergic receptor-dependent mechanism.

187 This suggests that signaling by beta-adrenergic receptors depends on temporal pattern of

188 our analysis suggests that activation of the beta-adrenergic receptor either via canonical (Gs-couple

189 tes synaptic plasticity, while activation of beta-adrenergic receptors elevates cAMP levels and modul

190 Using the beta-adrenergic receptor family as a model, we demonstra

191 tially reflecting down-regulation of cardiac beta-adrenergic receptor function in chronic hypoxia.

192 e suggested that rafts/caveolae may regulate beta-adrenergic receptor/Galpha(s) signaling, but underl

193 Therapeutic targeting of the beta-adrenergic receptors has recently shown remarkable

194 y the activation of excitatory alpha1A - and beta- adrenergic receptors in NPY/AgRP neurons, while PO

195 Triggering of beta-adrenergic receptors in adipocytes stimulates energ

196 he release of catecholamines, which activate beta-adrenergic receptors in cardiomyocytes and lead to

197 central regulator of signaling downstream of beta-adrenergic receptors in cardiomyocytes.

198 LTD is shifted by posttraining activation of beta-adrenergic receptors in fear conditioned mice, resu

199 h muscle tone in airways and the function of beta-adrenergic receptors in lungs and heart.

200 der hyperglycemic conditions and the role of beta-adrenergic receptors in regulating these responses.

201 Sympathetic stimulation of beta-adrenergic receptors in response to cold induces pr

202 In conclusion, activation of beta-adrenergic receptors in stratum lacunosum-molecular

203 salt hydrate (Sp-cAMPS) or activation of the beta-adrenergic receptor increased the phos pho ryl a ti

204 nt of rabbits with isoproterenol to activate beta-adrenergic receptors increased phosphorylation of S

205 ly, coactivation of these receptors with the beta-adrenergic receptors induced transient ERK signalin

206 Beta-adrenergic receptor induces cAMP/Protein kinase A (

207 iotensin II receptors blockade nor alpha and beta adrenergic receptors inhibition blunted leptin-indu

208 ong been established that stimulation of the beta-adrenergic receptor inhibits insulin-stimulated glu

209 when adrenergic stress or signaling through beta-adrenergic receptor is reduced.

210 on whether propranolol through inhibition of beta-adrenergic receptors is an appropriate therapeutic

211 inase gamma (PI3Kgamma) signaling engaged by beta-adrenergic receptors is pivotal in the regulation o

212 4 by phosphorylating the LTB4 receptor using beta adrenergic receptor kinase.

213 ng Gbetagamma using the C-terminal domain of beta-adrenergic receptor kinase (cbetaARK) resulted in c

214 beta-Adrenergic receptor kinase 1 (betaARK 1 or GRK2) me

215 and ERK1/2 activation through activation of beta-adrenergic receptor kinase 1.

216 -protein-coupled receptor kinase 3 (GRK3; or beta-adrenergic receptor kinase 2) was not only necessar

217 eceptor density and increases in Galphai and beta-adrenergic receptor kinase activities attenuate the

218 e Gbetagamma sink betaARK1-ct (C terminus of beta-adrenergic receptor kinase-1) was coexpressed with

219 s; Rab5 and Gbetagamma heterodimers; and the beta-adrenergic receptor kinase.

220 as also reversed by an inhibitory peptide to beta-adrenergic receptor kinase.

221 However, chronic stimulation of beta-adrenergic receptors leads to impaired cardiac func

222 Additionally, we report that beta-adrenergic receptors mediate the anxiety-like pheno

223 s greater in women than men and is, in part, beta-adrenergic receptor mediated.

224 However, beta-adrenergic receptor-mediated activation of GTP-Rac-

225 onsidered to be the predominant regulator of beta-adrenergic receptor-mediated enhancement of cardiac

226 Higher levels of GRK2 can impair beta-adrenergic receptor-mediated inotropic reserve and

227 ve beneficial effects unrelated to increased beta-adrenergic receptor-mediated signaling?

228 ha) as a direct transcriptional inhibitor of beta-adrenergic receptor-mediated, cyclic AMP-dependent

229 ve electrical stimulation (PNES) resulted in beta-adrenergic receptor-mediated-accumulation of B and

230 Our data suggest that the beta-adrenergic receptors offset alpha-adrenergic vasoco

231 ccur, in part, independently from alpha- and beta-adrenergic receptor-operated signaling and are inhi

232 Upon activation of beta-adrenergic receptors, phosphorylation of CaV1.2 cha

233 Downstream from beta-adrenergic receptors, PI3Kgamma was found to partic

234 hensive picture of the inactive state of the beta-adrenergic receptors, reconciling the crystal struc

235 ved in several important cellular processes (beta-adrenergic receptor recycling, centrosome amplifica

236 o, and treatment with propranolol to inhibit beta-adrenergic receptors reduced phosphorylation.

237 Stress hormone signaling through beta-adrenergic receptors regulates macrophage mechanoty

238 exocytosis when they bind to muscarinic and beta-adrenergic receptors, respectively.

239 ocytes, and restores the DHF-induced blunted beta-adrenergic receptor responsiveness.

240 e and epinephrine (NE/E) because stimulating beta-adrenergic receptors shortly after training can enh

241 During screening for noncanonical beta adrenergic receptor signaling pathways in human uro

242 Aging hearts exhibit impaired beta-adrenergic receptor signaling and LV dysfunction.

243 as well as amelioration of abnormal cardiac beta-adrenergic receptor signaling at 4 weeks post-MI.

244 These data reveal how baseline levels of beta-adrenergic receptor signaling can influence murine

245 bit PKA activity to test the hypothesis that beta-adrenergic receptor signaling causes cell death thr

246 eptor kinase-2 (GRK2)-mediated uncoupling of beta-adrenergic receptor signaling impairs inotropic res

247 mpartmentalization may also be important for beta-adrenergic receptor signaling in other cell types.

248 testinal metabolism via increased peripheral beta-adrenergic receptor signaling in peripheral organs,

249 a possible mechanism by which restoration of beta-adrenergic receptor signaling may protect the retin

250 These data show that differences caused by beta-adrenergic receptor signaling pathway gene polymorp

251 Full reconstitution of the beta-adrenergic receptor signaling pathway in heterologo

252 and feedback and feed-forward motifs of the beta-adrenergic receptor signaling pathway.

253 of prostate cancer, we show that endothelial beta-adrenergic receptor signaling via adrenergic nerve-

254 were assessed for alterations in calcium and beta-adrenergic receptor signaling, apoptosis, and cardi

255 e production and excessive signaling through beta-adrenergic receptor signaling, which is increased w

256 endothelin-1, renin-angiotensin, and cardiac beta-adrenergic receptor signaling, which were not inhib

257 r near key protein binding sites critical to beta-adrenergic receptor signaling.

258 Bisoprolol restored RV beta-adrenergic receptor signaling.

259 ulated in HF patients, causing dysfunctional beta-adrenergic receptor signaling.

260 ty in brown adipocytes through modulation of beta-adrenergic receptor signaling.

261 ivator Crtc3 promotes obesity by attenuating beta-adrenergic receptor signalling in adipose tissue.

262 in chronic cold adaptation in the absence of beta-adrenergic receptor signalling.

263 at for the same receptor molecule (e.g., the beta-adrenergic receptor), some agonists have a propensi

264 ce of AC6 was associated with a 48% decay in beta-adrenergic receptor-stimulated cAMP production in c

265 ements of cell shortening revealed augmented beta-adrenergic receptor-stimulated cardiomyocyte contra

266 ) adipocytes, insulin was unable to suppress beta-adrenergic receptor-stimulated glycerol release.

267 Chronic ethanol feeding suppressed beta-adrenergic receptor-stimulated lipolysis in both in

268 sing aortic constriction combined with daily beta-adrenergic receptor stimulation (ACi) and show that

269 reezing method to study the effects of acute beta-adrenergic receptor stimulation (through isoprotere

270 tion potential duration, supersensitivity to beta-adrenergic receptor stimulation and Ca(2+) mishandl

271 egulation in mouse hearts undergoing chronic beta-adrenergic receptor stimulation and in a rat model

272 timulated Ca(2)(+) current in the absence of beta-adrenergic receptor stimulation and in voltage-depe

273 ate and attenuate the deleterious effects of beta-adrenergic receptor stimulation in septic shock.

274 se previous experimental studies showed that beta-adrenergic receptor stimulation increases the rate

275 vivo myocardial function was unchanged, but beta-adrenergic receptor stimulation of cardiac inotropy

276 ospholamban, a process that does not require beta-adrenergic receptor stimulation or protein kinase A

277 st experimental demonstration that localized beta-adrenergic receptor stimulation produces spatiotemp

278 sults in spontaneous SR Ca(2+) releases upon beta-adrenergic receptor stimulation with isoproterenol

279 Local beta-adrenergic receptor stimulation with noradrenaline

280 in phospholamban phosphorylation produced by beta-adrenergic receptor stimulation, phosphodiesterase

281 epolarization phenotype, particularly during beta-adrenergic receptor stimulation, remain unclear.

282 els the changes observed experimentally with beta-adrenergic receptor stimulation.

283 associated with excess Ca2+ influx and acute beta-adrenergic receptor stimulation.

284 e 4B) is a key negative regulator of cardiac beta-adrenergic receptor stimulation.

285 d secretion of alpha-amylase secretion after beta-adrenergic receptor stimulation.

286 CaR potency as well as selectivity over the beta-adrenergic receptor subtypes.

287 ogression in part owing to uncoupling of the beta-adrenergic receptor system.

288 ated through signaling pathways identical to beta-adrenergic receptors, thus providing support that i

289 del the flow of spatial information from the beta-adrenergic receptor to MAPK1,2 through the cAMP/PKA

290 lting from impaired signal transduction from beta-adrenergic receptors to adenylate cyclase.

291 ry pathways and discovered that NA activates beta-adrenergic receptors to boost LTP maintenance in ar

292 cellular populations that express different beta-adrenergic receptors to induce beige adipogenesis.

293 aimed to examine whether the ability of the beta-adrenergic receptors to offset the transduction of

294 PLCepsilon in response to the stimulation of beta-adrenergic receptors, translocating the complex to

295 of the L-type current by stimulation of the beta-adrenergic receptor was unaffected in vivo and in c

296 iomas are reported to express high levels of beta adrenergic receptors, we examined the expression of

297 ion of PKA through G(s)-coupled dopamine and beta-adrenergic receptors, which regulate the late-phase

298 prediction that a complete antagonist of the beta-adrenergic receptor will likely block long-lasting

299 Blockade of beta-adrenergic receptors with atenolol abolished the pu

300 Stimulation of Galphas-coupled beta-adrenergic receptors with isoproterenol induced PKA