ライフサイエンスコーパス: adrenergic

1 beta-Adrenergic activation in brown adipocytes results in a d

2 The precise molecular mechanisms of beta-adrenergic activation of cardiac CaV1.2, however, are in

3 deleting Hdac1 significantly enhances, beta-adrenergic activation-induced BAT-specific gene expressi

4 ssary to optimize cardiac contractility upon adrenergic activation.

5 change in response to cold exposure or beta-adrenergic activation.

6 neous adipose tissue, EAT showed an enhanced adrenergic activity demonstrated by the increased catech

7 ic events, and paradoxical responses to beta-adrenergic agents.

8 ings of increased risk associated with beta2-adrenergic agonist agents together with stress related t

9 proterenol, a rapidly acting peripheral beta-adrenergic agonist akin to adrenaline, or saline.

10 hallenge of Zmpste24(-/-) mice with the beta-adrenergic agonist isoproterenol did not trigger ventric

11 levels that were pre-elevated with the beta-adrenergic agonist isoproterenol.

12 proterenol, a rapidly acting peripheral beta-adrenergic agonist similar to adrenaline, to induce sens

13 shown that combinations of long-acting beta2-adrenergic agonists (LABAs) and long-acting muscarinic a

14 e computed bias factors for a number of beta-adrenergic agonists by comparing BRET assays of receptor

15 which corticosteroids and long-acting beta2 -adrenergic agonists confer protection against pathologic

16 oxetine than for the extended-release alpha2-adrenergic agonists guanfacine or clonidine (no studies)

17 kers, 4.01 (CrI, 0.48 to 7.43); 1995: alpha2-adrenergic agonists, 5.64 (CrI, 1.73 to 9.50); 1999: pro

18 nses to glutamatergic, lysophosphatidic, and adrenergic agonists.

19 llular signal-regulated kinase) activity via adrenergic alpha1 and alpha2 receptors.

20 -, delta-, and kappa-opioid receptors and by adrenergic alpha2A receptors in the spinal cord.

21 D1)) may contribute to drug seeking via beta-adrenergic and 5-HT neurotransmission in DH.

22 n ED1 following 10 mg/kg S-propranolol (beta-adrenergic and 5-HT1A/1B receptor antagonist), R-propran

23 Adrenergic and cardiovagal function tests including HUT

24 protein-coupled receptors (GPCRs), including adrenergic and endothelin (ET) receptors, after elevated

25 Thus, CB1 receptors on adrenergic and noradrenergic cells provide previously un

26 ht or flight" through activation of the beta-adrenergic and protein kinase A (PKA) signaling pathway.

27 evels through interaction with dopaminergic, adrenergic and serotonergic system components; it is the

28 s action required Gialpha-coupled D2, alpha2-adrenergic, and 5HT1A receptors, respectively.

29 Sympathetic adrenergic- and non-adrenergic-dependent contributions t

30 gn, we orally administered either the alpha2-adrenergic antagonist yohimbine (increasing noradrenergi

31 ugh it is the most important target for beta-adrenergic antagonists, such as beta-blockers, relativel

32 is study aimed to elucidate the role of beta-adrenergic (beta-AR) stimulation in mediating the contri

33 n adipocytes, catecholamines target the beta-adrenergic (beta-AR)/cAMP pathway to activate cytosolic

34 k output following either placebo or alpha1 -adrenergic blockade (prazosin; 0.05 mg kg( -1) ).

35 sity exercise, and administration of alpha1 -adrenergic blockade elevated FMD (P = 0.032).

36 sity exercise, and administration of alpha1 -adrenergic blockade resulted in an increase in flow-medi

37 did not induce anaphylaxis, even after beta-adrenergic blockade, and did not deplete FcgammaRIII or

38 rcise at sea level was abolished via alpha1 -adrenergic blockade.

39 ith and without administration of an alpha1 -adrenergic blockade.

40 aRIII dependent and greatly enhanced by beta-adrenergic blockade.

41 and this decrease was abolished with alpha1 -adrenergic blockade.

42 ith and without administration of an alpha1 -adrenergic blockade.

43 initially thought to be harmful in HF, beta-adrenergic blockers (beta-blockers) have consistently be

44 of carvedilol (independent of its alpha/beta-adrenergic blocking activity), flecainide, and riluzole;

45 namic electrophysiological responses to beta-adrenergic challenge, have therapeutic implications for

46 dulla (AM) represent the main neuroendocrine adrenergic component and are believed to differentiate f

47 ired dilator responses, a modest increase in adrenergic constriction combined with an elevated thromb

48 LV twist mechanics may be more sensitive to adrenergic control in males than in females.

49 Differences in cardiac autonomic and adrenergic control may contribute to sex differences in

50 re fundamentally regulated by differences in adrenergic control.

51 Sympathetic adrenergic- and non-adrenergic-dependent contributions to reflex cutaneous v

52 ed as an alternative to the recommended beta-adrenergic drugs for supporting endotoxin-induced myocar

53 h combined therapeutic approaches to correct adrenergic dysfunction, elevated oxidant stress and incr

54 lation elicited by other GPCRs such as beta2-adrenergic, FSH and CXCR4 receptors, but does not affect

55 An altered adrenergic function has been reported in GAD, however di

56 ucleotide polymorphisms (SNPs) involved with adrenergic function were genotyped; adrenergic receptors

57 h five integral membrane proteins: the beta2-adrenergic G protein-coupled receptor (beta2AR), the pep

58 rotein whose epitopes are known, human beta2 adrenergic G-protein-coupled receptor, with promising re

59 cological studies revealed the prevention of adrenergic-induced arrhythmias by beta-blockers (propran

60 Dobutamine is the currently recommended beta-adrenergic inotropic drug for supporting sepsis-induced

61 inkage could be related to innervations from adrenergic input and the hypothalamus-pituitary-adrenal

62 At low adrenergic levels, and those mimicking heart failure, di

63 ve mechanism of action to traditional alpha1-adrenergic ligands, yet there is little information desc

64 -19-independent pathway requiring an alpha2A-adrenergic-like octopamine (OA) receptor, OCTR-1, and a

65 Herein, we explored a potential non-adrenergic mechanism by which Lcn2 regulates thermogenes

66 Finally, Rab9-GDP expression did not affect adrenergic-mediated calcium response but abolished recep

67 es of TnI and MyBP-C phosphorylation in beta-adrenergic-mediated enhancement of cardiac function, tra

68 These findings suggest that adrenergic-mediated loss of MZ B cells contributes to th

69 We further demonstrate that adrenergic modulation of Kv1.1 was mediated by the signa

70 elial beta-adrenergic receptor signaling via adrenergic nerve-derived noradrenaline in the prostate s

71 urther highlighting the critical role of the adrenergic nervous system in this disorder.

72 ow coupled with an increased reliance on non-adrenergic neurotransmitters.

73 red intracavernous pressure and impaired non-adrenergic non-cholinergic-mediated relaxation in the pe

74 se, and the interactions between the alpha1 -adrenergic pathway and endothelial function.

75 gulation of adaptive thermogenesis via a non-adrenergic pathway.

76 nd high altitude are mediated via an alpha1 -adrenergic pathway.

77 drenergic signaling by administration of the adrenergic prodrug dipivefrin at reactivation increased

78 Subsequently, we identified the beta2 adrenergic receptor (ADRB2) as a downstream target for P

79 Sustained beta3 adrenergic receptor (ADRB3) activation simultaneously up

80 eiging response: cold temperatures and beta3-adrenergic receptor (Adrb3) agonists.

81 vasopressin receptor (V1A-R) but not alpha1 adrenergic receptor (alpha1-AR), suggesting that GPCR pr

82 rect interaction between APP and the alpha2A-adrenergic receptor (alpha2AAR) that occurs at the intra

83 handgrip-exercise ischaemia (PEI) and beta1 -adrenergic receptor (AR) blockade.

84 predicting activation pathways of the beta 2-adrenergic receptor (beta 2-AR), folding of the FiP35 WW

85 We used beta-adrenergic receptor (beta-AR) signaling as a prototype t

86 tumor microenvironment is regulated by beta2-adrenergic receptor (beta-AR) signaling in host immune c

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

88 s myocardial calcium transients through beta-adrenergic receptor (beta-AR)-mediated phosphorylation o

89 The beta1-adrenergic receptor (beta1AR) is a G protein-coupled rec

90 The beta1 adrenergic receptor (beta1AR) is recognized as a classic

91 t elevation of phosphorylation of the beta2 -adrenergic receptor (beta2 AR) at both the protein kinas

92 timulated by two Gs-coupled receptors, beta2-adrenergic receptor (beta2-AR) and D1 dopamine receptor

93 The beta-2 adrenergic receptor (beta2AR) agonist formoterol induces

94 pertrophy stimulated by clenbuterol, a beta2-adrenergic receptor (beta2AR) agonist, was significantly

95 -15) is an allosteric modulator of the beta2 adrenergic receptor (beta2AR) that was recently isolated

96 aging, we examine TM6 movements in the beta2 adrenergic receptor (beta2AR) upon exposure to orthoster

97 ine 2B receptor (A2BR), but not of the beta2 adrenergic receptor (beta2AR), leading to an enhanced, a

98 g to analyze GRK5 interaction with the beta2-adrenergic receptor (beta2AR).

99 population of Galphai and its coupled beta2-adrenergic receptor (betaAR), are localized to caveola d

100 t, expended less energy in response to beta3-adrenergic receptor activation, and were more insulin re

101 or in combination with a long-acting beta2 -adrenergic receptor agonist (LABA) on GCM in the bronchi

102 rality were treated with the selective beta3 adrenergic receptor agonist CL 316, 243 and underwent me

103 Treatment with the beta3-adrenergic receptor agonist CL316,243 increased Cx43 exp

104 In humans, the alpha2-adrenergic receptor agonist clonidine increases decisive

105 Salmeterol is a long-acting beta2-adrenergic receptor agonist used to treat chronic obstru

106 rine, a catecholamine that binds to the beta-adrenergic receptor and activates the cAMP-PKA-dependent

107 beta-adrenergic receptor antagonism after experimental stroke

108 1 (CRF1) antagonist (antalarmin), and alpha2-adrenergic receptor antagonist (yohimbine; used as a pha

109 4 h or by intravenous infusion of the alpha-adrenergic receptor antagonist phentolamine for only 30

110 We find that administration of the beta-adrenergic receptor antagonist propranolol before memory

111 Orthosteric beta-adrenergic receptor antagonists, known as beta-blockers,

112 teracts with the BiOctR, DmOctR, and alpha2C-adrenergic receptor at an allosteric site.

113 In contrast, during beta1 -adrenergic receptor blockade, LV apical rotation, twist

114 , ganglionic-blocker administration or beta2-adrenergic receptor blockade.

115 ing post-exercise ischaemia (PEI) and beta1 -adrenergic receptor blockade.

116 The structures of beta2-adrenergic receptor bound with a variety of ligands prov

117 nalysis suggests that activation of the beta-adrenergic receptor either via canonical (Gs-coupled) or

118 amyloid precursor protein modulates alpha2A-adrenergic receptor endocytosis and signaling through di

119 y reflecting down-regulation of cardiac beta-adrenergic receptor function in chronic hypoxia.

120 nsistent with the crystal structure of beta2 adrenergic receptor in complex with Gs Conformational ch

121 onto the extracellular domain of the Beta-2 adrenergic receptor in HEK293T cells, followed by incuba

122 ssociated with significant changes in beta2 -adrenergic receptor phosphorylation at protein kinase A

123 gnaling profiles of 28 variants of the beta2-adrenergic receptor reveals three clearly distinct pheno

124 further demonstrate that the endosomal beta2-adrenergic receptor signal confers uniformity on the dow

125 mpacts of high-fat diet (HFD) on the insulin-adrenergic receptor signal network in hearts.

126 e recently uncovered an insulin receptor and adrenergic receptor signal network in the heart.

127 ction of caveolin-3 is able to confine beta2 adrenergic receptor signaling and restore myocyte contra

128 ostate cancer, we show that endothelial beta-adrenergic receptor signaling via adrenergic nerve-deriv

129 d in HF patients, causing dysfunctional beta-adrenergic receptor signaling.

130 function and is mediated, in part, by beta1-adrenergic receptor signaling.

131 fat diet (HFD) feeding on the cardiac beta2 -adrenergic receptor signalling and the impacts on cardia

132 -coupled receptor (GPCR) and the predominant adrenergic receptor subtype in the heart, where it media

133 gest that protein kinase C modulates alpha1B-adrenergic receptor transfer to late endosomes and that

134 ction that a complete antagonist of the beta-adrenergic receptor will likely block long-lasting LTP i

135 the delta-opioid receptor, but not the beta2-adrenergic receptor, defining a role for CLCs in the upt

136 rescent proteins and four GPCRs: the alpha2A-adrenergic receptor, GABAB, cannabinoid receptor type 1

137 cently labeled Galphai1 subunits and alpha2A-adrenergic receptor, GABAB, or dopamine receptor type 2

138 dothelial Adrb2, the gene encoding the beta2-adrenergic receptor, leads to inhibition of angiogenesis

139 ng (13)C methyl methionine NMR for the beta1-adrenergic receptor, we identify ligand efficacy-depende

140 d by acute treadmill exercise through a beta-adrenergic receptor-dependent mechanism.

141 an architecture similar to that of the beta2-adrenergic receptor-GS complex, including a flexible alp

142 raffic were investigated by studying alpha1B-adrenergic receptor-Rab protein interactions, using Fors

143 gonist-GPCR complex of iodopindolol and beta-adrenergic receptor.

144 The beta1-adrenergic-receptor (ADRB1) antagonist metoprolol reduce

145 or cervical ganglion (SCG) neurons expressed adrenergic receptors (activated by epinephrine) and the

146 aluated the associations of gene variants in adrenergic receptors (ADRs) with GAD, with the involveme

147 In contrast, activation of alpha1B-adrenergic receptors (alpha1B-ARs) induced transient inh

148 lutionary precursor to the vertebrate alpha2-adrenergic receptors (alpha2-ARs) based upon sequence si

149 gulation of cell surface transport of alpha2-adrenergic receptors (alpha2-ARs) by GGA3 (Golgi-localiz

150 iprocal down-regulation occurs between beta1-adrenergic receptors (ARs) and the cardioprotective sphi

151 Agonist-triggered downregulation of beta-adrenergic receptors (ARs) constitutes vital negative fe

152 cular myocyte expresses all 5 of the cardiac adrenergic receptors (ARs), beta1, beta2, beta3, alpha1A

153 Noradrenaline acts through adrenergic receptors (ARs), of which beta2-adrenergic re

154 re, we hypothesized that activation of beta1-adrenergic receptors (beta1ARs) localized to ghrelin cel

155 beta1-adrenergic receptors (beta1ARs) mediate catecholamine ac

156 by the sympathetic nervous system via beta3-adrenergic receptors (beta3-AR).

157 beta-adrenergic receptors (betaARs) are critical regulators o

158 Beta adrenergic receptors (betaARs) are G-protein-coupled rec

159 h adrenergic receptors (ARs), of which beta2-adrenergic receptors (betaARs) are of particular importa

160 In heart failure, the beta-adrenergic receptors (betaARs) become desensitized and u

161 Activation of beta-adrenergic receptors (betaARs) enhances both the inducti

162 Stimulation of beta-adrenergic receptors (betaARs) provides the most efficie

163 norepinephrine, through its actions on beta-adrenergic receptors (betaARs), modulates aversive memor

164 ved with adrenergic function were genotyped; adrenergic receptors alpha(1A) (ADRA1A), alpha(2A) (ADRA

165 It is known that beta-adrenergic receptors and NA can boost LTP maintenance by

166 n dissociation from the alpha1A- and alpha1B-adrenergic receptors and noncompetitively inhibit recept

167 The alpha1-adrenergic receptors are targets for a number of cardiov

168 Adrenergic receptors are the primary target for GRK2 act

169 Upon agonist stimulation, alpha1B-adrenergic receptors couple to Gq proteins, calcium sign

170 eatly reduced, suggesting that activation of adrenergic receptors in DRG neurons is preferentially li

171 because of, for example, activation of beta1-adrenergic receptors in myocardium.

172 activation of excitatory alpha1A - and beta- adrenergic receptors in NPY/AgRP neurons, while POMC neu

173 Sympathetic stimulation of beta-adrenergic receptors in response to cold induces prolife

174 Additionally, we report that beta-adrenergic receptors mediate the anxiety-like phenotype

175 l of arousal by selectively targeting alpha2 adrenergic receptors on LC neurons, resulting in reduced

176 ycling by activation of alpha1- and/or beta3-adrenergic receptors or the SERCA2b-RyR2 pathway stimula

177 When alpha1B-adrenergic receptors that had been mutated at protein ki

178 NE enhances thermogenesis through beta3-adrenergic receptors to activate brown adipose tissue an

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

180 ular populations that express different beta-adrenergic receptors to induce beige adipogenesis.

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

182 odopsin (visual receptor), opioid receptors, adrenergic receptors, adenosine receptors, dopamine rece

183 mpal LTP, decreased neuronal levels of beta2-adrenergic receptors, and activated microglia in wt mice

184 tested for the beta2-, alpha1-, and alpha2- adrenergic receptors, and adenosine type 1 receptor (A1R

185 through signaling pathways identical to beta-adrenergic receptors, thus providing support that inhibi

186 We observed that the content of beta2-adrenergic receptors, which are mainly expressed in skel

187 s also shown to be a modulator of the alpha1-adrenergic receptors, which suggests a general lack of s

188 tion of presynaptic TRPV1 channels by alpha2 adrenergic receptors.

189 ile POMC neurons are inhibited via alpha2A - adrenergic receptors.

190 and could be reversed by antagonism of beta3 adrenergic receptors.

191 teric modulation of the alpha1A- and alpha1B-adrenergic receptors.

192 that it was mediated by activation of alpha2 adrenergic receptors.

193 within a single subfamily, such as the nine adrenergic receptors.

194 logical inhibition of muscarinic and/or beta-adrenergic receptors.

195 ion describing this drug class at the alpha1-adrenergic receptors.

196 , and is induced upon the activation of beta-adrenergic receptors.

197 ne, histamine, melatonin, acetylcholine, and adrenergic receptors.

198 bine, consistent with contribution of alpha2 adrenergic receptors.

199 We determined that acute beta-adrenergic regulation does not require any combination o

200 own individually not to be required for beta-adrenergic regulation of CaV1.2 current (17-mutant).

201 tes to contractile dysfunction and decreased adrenergic reserve in response to acute stress.

202 ptor kinase site serine 355/356 and impaired adrenergic reserve when compared with mice fed on normal

203 deletion of the beta2 AR led to a normalized adrenergic response and preserved cardiac contractile re

204 vascularized adipose tissue, capable of beta-adrenergic-responsive glucose uptake.

205 The cardiac potassium channel, IKr, and the adrenergic-sensitive cardiac potassium current, IKs, are

206 howed no HTN-related difference in cutaneous adrenergic sensitivity (logEC50 ; NTN: -7.4 +/- 0.3 log

207 ediated by an increase in cutaneous vascular adrenergic sensitivity and a greater contribution of non

208 flex cutaneous vasoconstriction and vascular adrenergic sensitivity were assessed pharmacologically u

209 It is concluded that activation of alpha2A-adrenergic signal in chondrocytes promotes TMJ degenerat

210 Enhanced beta-adrenergic signaling and higher sensitivity to catechola

211 l follicle cells (the receptor for receiving adrenergic signaling and inducing Mmp2 activation).

212 We investigated beta-adrenergic signaling and TTS cardiomyocyte function.

213 hese findings uncover a critical K(+)-Ca(2+)-adrenergic signaling axis that acts to dampen thermogene

214 By contrast, enhancement of adrenergic signaling by administration of the adrenergic

215 events Ca(2+) leakage, or blocking the beta2-adrenergic signaling cascade reduced betaAPP processing

216 yR occur downstream of Abeta through a beta2-adrenergic signaling cascade that activates PKA.

217 D Atomic force microscopy revealed that beta-adrenergic signaling enhances both the number of desmogl

218 Chronic behavioral stress and beta-adrenergic signaling have been shown to promote cancer p

219 ng initial abstinence involves 5-HT and beta-adrenergic signaling in female DH, but only 5-HT signali

220 n was completely blunted by blockade of beta-adrenergic signaling in MCF-7 cells, indicating that cat

221 TTS, to test the hypothesis of altered beta-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), a

222 Enhanced beta-adrenergic signaling in TTS-iPSC-CMs under catecholamine

223 HDAC2 was induced by beta-adrenergic signaling in vitro and in mouse xenografts.

224 At cellular levels, adrenergic signaling increases dendrite excitability, bu

225 Preclinical studies have suggested that beta-adrenergic signaling is involved in pancreatic cancer pr

226 The data suggest new paradigms in cardiac adrenergic signaling mechanisms.

227 owed that chronic behavioral stress and beta-adrenergic signaling promote angiogenesis and prostate c

228 Mechanistically, beta2 adrenergic signaling reinforced an autocrine feedback lo

229 Notably, HDAC2 is necessary for beta-adrenergic signaling to induce angiogenesis.

230 P1 act downstream of CREB activation in beta-adrenergic signaling to promote cancer progression.

231 interplay between amyloid beta (Abeta), beta-adrenergic signaling, and altered Ca(2+) signaling via l

232 zation by beta2AR has broad implications for adrenergic signaling, cross-talk with other signaling pa

233 ltage-dependent calcium channels and dampens adrenergic signaling, thereby attenuating lipolysis and

234 lx, which is stabilized in response to beta3-adrenergic signaling, to increase thermogenic gene expre

235 and is translationally upregulated by beta3-adrenergic signaling-mediated suppression of the transla

236 is unknown whether it is necessary for beta-adrenergic signaling-promoted cancer progression.

237 loproteinases (Mmps), steroid signaling, and adrenergic signaling.

238 ing protein (CREB) that is activated by beta-adrenergic signaling.

239 and emotional states involving activation of adrenergic signaling.

240 t affect hepatic insulin sensitivity or beta-adrenergic signaling.

241 mental mechanistic insights into subcellular adrenergic signalling in normal and pathological cardiac

242 sting that early intervention in the insulin-adrenergic signalling network might be effective in prev

243 sex differences in LV mechanics with altered adrenergic stimulation achieved through post-handgrip-ex

244 ractive effect between oil-exposure and beta-adrenergic stimulation and suggests if animals achieve v

245 Adrenergic stimulation can increase BAT (18)F-FDG uptake

246 a blunted cardiac inotropic response to beta-adrenergic stimulation despite normal cardiac contractil

247 Cold exposure or beta-adrenergic stimulation favors the active thermogenic sta

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

249 nics may be more sensitive to alterations in adrenergic stimulation in males, but more highly influen

250 tractile function at rest and in response to adrenergic stimulation in obese swine after myocardial i

251 animals achieve very large increases in beta-adrenergic stimulation it could play a compensatory role

252 cy response; (4) inotropic responses to beta-adrenergic stimulation mediated via canonical beta1- and

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

254 PKA phosphorylation sites in alpha1C in beta-adrenergic stimulation of CaV1.2, and show that phosphor

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

256 nge in fluorescence intensity in response to adrenergic stimulation of cells, which corresponded to t

257 Adrenergic stimulation promotes lipid mobilization and o

258 beta-Adrenergic stimulation rapidly activated PKA, which led

259 emonstrating a defect in the ability of beta-adrenergic stimulation to regulate sarcoplasmic reticulu

260 Pharmacological and physiological beta-adrenergic stimulation upregulates FGF10 levels and prom

261 displayed a reduced contractile response to adrenergic stimulation when compared with those of contr

262 me-averaged [Ca(2+) ]i was increased by beta-adrenergic stimulation with isoprenaline and increased i

263 rdiac functional reserve in response to beta-adrenergic stimulation without significant alteration of

264 fficient to regulate respiration during beta-adrenergic stimulation, arguing against intracrine contr

265 However, with increased heart rate or beta-adrenergic stimulation, cTnIS200D mice had less enhanced

266 amplitude-frequency relationship and in beta-adrenergic stimulation, including decreasing and increas

267 les compared to females during reductions to adrenergic stimulation, providing preliminary evidence t

268 are selectively preserved under a sustained adrenergic stimulation, which results in the down-regula

269 evant source of intracellular NO during beta-adrenergic stimulation, while no evidence for a mitochon

270 ranscription of these genes independently of adrenergic stimulation.

271 d cardiac contractile reserve in response to adrenergic stimulation.

272 ecies and induction of autophagy during beta-adrenergic stimulation.

273 ong-term potentiation, and responsiveness to adrenergic stimulation.

274 brown adipocyte function in response to beta-adrenergic stimulation.

275 ckout hearts failed to functionally adapt to adrenergic stimulation.

276 re myocyte contractility in response to beta adrenergic stimulation.

277 by voluntary exercise and by persistent beta-adrenergic stimulation.

278 ribute to the net stimulatory effect of beta-adrenergic stimulation.

279 d early-after-depolarisations following beta-adrenergic stimulation.

280 pocyte differentiation and activated by beta-adrenergic stimulation.

281 (MyBP-C), are phosphorylated following beta-adrenergic stimulation; however, their relative contribu

282 These data highlight the potential of adrenergic stress and norepinephrine-driven beta-AR sign

283 creased propensity to arrhythmias under beta-adrenergic stress conditions.

284 d genetic (beta2-AR knockout mice) to reduce adrenergic stress signaling in two widely studied precli

285 rt under basal conditions and following beta-adrenergic stress.

286 urther demonstrate an important role for non-adrenergic sympathetic co-transmitters in mediating the

287 -7.5 +/- 0.3 log M; P = 0.84); however, non-adrenergic sympathetic co-transmitters mediated a signif

288 ensitivity and a greater contribution of non-adrenergic sympathetic co-transmitters.

289 reased expression of proapototic (BMF, BIM), adrenergic (TH), and cell-cycle genes (e.g., CDC25A, CDK

290 on is enhanced in cirrhosis due to augmented adrenergic tone and modulated by treatment with beta-blo

291 ntricular action potentials during high beta-adrenergic tone.

292 ntravascular ATP attenuate sympathetic alpha-adrenergic vasoconstriction (sympatholysis).

293 Next, spironolactone inhibited alpha-adrenergic vasoconstriction in arterioles from mice and

294 of EDH-like vasodilatation can blunt alpha1 -adrenergic vasoconstriction in contracting skeletal musc

295 sis that the ability of ATP to blunt alpha1 -adrenergic vasoconstriction in resting skeletal muscle w

296 Impaired postsynaptic alpha1-adrenergic vasoconstriction in young adults with VVS can

297 ate that intravascular ATP modulates alpha1 -adrenergic vasoconstriction via pathways independent of

298 contracting skeletal muscle to blunt alpha1 -adrenergic vasoconstriction.

299 ot alter the ability of ATP to blunt alpha1 -adrenergic vasoconstriction.

300 maintained the ability to attenuate alpha1 -adrenergic vasoconstriction.