ライフサイエンスコーパス: catecholamine

1 ls of mammals (acetylcholine, adenosine, and catecholamines).

2 and other beta-AR signalling hormones (i.e. catecholamines).

3 retaining the intrinsic adhesive function of catecholamine.

4 y stopped the study drug and started another catecholamine.

5 cence microscopy and amperometry of released catecholamine.

6 , increasing bioavailability of cortisol and catecholamine.

7 beta-blockers, intra-aortic balloon pump, or catecholamines.

8 thereby minimizing the detrimental effect of catecholamines.

9 by a drastic fall in the quantal release of catecholamines.

10 transformation overlaps with those of other catecholamines.

11 contractility and vascular responsiveness to catecholamines.

12 vity COMT, signifying impaired catabolism of catecholamines.

13 mpathetic activity and increased circulating catecholamines.

14 contractility and remodeling in response to catecholamines.

15 actile capacity but a diminished response to catecholamines.

16 Catecholamine-0-methyl-transferase (COMT) gene variation

17 imals, defect of the metabolically resistant catecholamine (11)C-hydroxyephedrine was smaller than ep

18 ricle, P = 0.004), whereas defect of a third catecholamine, (11)C-phenylephrine, which is sensitive t

19 tients with severe shock requiring high-dose catecholamines 3-24 hours post-cardiac surgery who were

20 eta1-adrenergic receptors (beta1ARs) mediate catecholamine actions in cardiomyocytes by coupling to b

21 molecular link that couples the coordinated catecholamine activation of the PKA pathway and of lipid

22 rthermore, a pharmacological manipulation of catecholamine activity affected learning rate following

23 Admission plasma levels of catecholamines (adrenaline, noradrenaline) and biomarker

24 sychostimulant medication, most commonly the catecholamine agonist methylphenidate, is the most effec

25 Elevated catecholamines also allow for maintenance of a normal fe

26 sed this approach to simultaneously quantify catecholamine and M-ENK fluctuations in live tissue.

27 uctions in levels of glucagon, cortisol, and catecholamine and the sympathetic nerve responses to hyp

28 es the release of neurotransmitters, such as catecholamines and acetylcholine, directly into the vici

29 s is associated with increased production of catecholamines and corticosteroids, decreased formation

30 ranin A (CHGA) is co-stored/co-secreted with catecholamines and crucial for secretory vesicle biogene

31 the Ca(2+) channel domain compared with the catecholamines and forskolin.

32 1) a high-affinity state where responses to catecholamines and other agonists (e.g., cimaterol) are

33 ficacy and can be used in detection of other catecholamines and phenolic neurochemicals.

34 RC1 that is required for adipose browning by catecholamines and provides potential therapeutic strate

35 Catecholamines and serotonin cause arrhythmias in atrial

36 sm of energy reserves through the release of catecholamines and subsequent activation of protein kina

37 phages do not synthesize relevant amounts of catecholamines, and hence, are not likely to have a dire

38 f adipocyte-expressed beta3 adrenoceptors by catecholamines, and identified eosinophils as a novel so

39 ncluding various ways to measure heart rate, catecholamines, and sympathetic neural activity.

40 hering to the electrode and screening of the catecholamine-aptamer electrostatic interactions, allows

41 rovides strong neuroanatomical evidence that catecholamines are important modulators of both auditory

42 r of individual and binary mixtures of three catecholamines are investigated using gold microelectrod

43 In this study, we describe the role of catecholamines (as mediators of the sympathetic nervous

44 tivity and revealed heterogeneous release of catecholamine at the chromaffin cell surface.

45 ydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, protected mice against EAE.

46 Furthermore, catecholamine levels, catecholamine biosynthetic enzymes, and sympathetic nerv

47 eased catecholamine levels and expression of catecholamine biosynthetic enzymes.

48 erstand the role of genetic variation in the catecholamine biosynthetic pathway for control of human

49 ay also contribute to the expression of this catecholamine biosynthetic trait.

50 ing etiology is likely related to release of catecholamines, both locally in the myocardium and in th

51 sis and tended to be more rapidly weaned off catecholamines but had more frequent hypophosphatemia, m

52 al behaviors in vertebrates are modulated by catecholamine (CA; dopamine, norepinephrine, epinephrine

53 Costimulation with catecholamines, carcinoembryonic antigen cell adhesion m

54 c question regarding how glucocorticoids and catecholamines cause leukocyte demargination.

55 mice exhibit an impaired cardiac response to catecholamine challenge.

56 blood pressure (SBP) with decreased urinary catecholamine compared to diabetic Cav2.2(+/+) mice.

57 hese vesicles contain about one tenth of the catecholamine compared with adrenal chromaffin vesicles.

58 cells in bone marrow with increased urinary catecholamine concentrations at diagnosis.

59 s study is that increases in MSNA and plasma catecholamine concentrations did not differ between youn

60 sympathetic nerve activity (MSNA) and plasma catecholamine concentrations in healthy young and aged i

61 We propose that sustained high catecholamine concentrations observed in the IUGR fetus

62 oxygen concentrations increase fetal plasma catecholamine concentrations, which lower fetal insulin

63 onist responses at the primary high-affinity catecholamine conformation while also exerting agonist e

64 Catecholamine-containing cells were not found in any of

65 ied the mechanism of VIEC by quantifying the catecholamine content in single vesicles isolated from p

66 rter 2 and was associated with reduced renal catecholamine content.

67 used, allowing us to quantify the vesicular catecholamine content.

68 These changes in catecholamines could be rescued by re-expression of DJ-1

69 observed postnatal lethality occurs due to a catecholamine deficiency and subsequent heart failure.

70 d that ageing upregulates genes that control catecholamine degradation in an NLRP3 inflammasome-depen

71 The colligative properties of ATP and catecholamines demonstrated in vitro are thought to be r

72 These cellular catecholamine-dependent responses were mainly mediated b

73 nvolved behavioral responses to experimental catecholamine depletion (CD).

74 hyl-paratyrosine (AMPT) over 24 h to achieve catecholamine depletion in a randomized, crossover study

75 ated with a dysregulated dopamine system and catecholamine depletion led to reward-processing deficit

76 ation in the sham condition and unrelated to catecholamine depletion.

77 al tools like alpha-methyl-p-tyrosine (AMPT, catecholamine depletor), p-chlorophenylalanine (serotoni

78 neurotransmitter imbalance, particularly the catecholamines dopamine (DA) and noradrenaline.

79 s the evidence implicating disruption of the catecholamines (dopamine and noradrenaline) and review t

80 These findings suggest that catecholamines drive a feedforward loop, whereby upregul

81 netics of local myocardial delivery of small catecholamine drugs in large animal models.

82 ities of systemic and uterine vasculature to catecholamines during pregnancy and the role of fetal in

83 d with reduced contractility and response to catecholamines during steady-state pacing, likely becaus

84 es an alternative source of locally produced catecholamines during the thermogenic process.

85 se of this study was to identify the role of catecholamine dysfunction and its relation to behavioral

86 Our results fill this void by showing that catecholamines enhance the precision of encoding cortica

87 sed biases were altered independently by the catecholamine enhancer melthylphenidate.

88 f the syb2 TMD in fusion pores formed during catecholamine exocytosis in mouse chromaffin cells.

89 uency stimulation in turn elicits sufficient catecholamine exocytosis to set basal sympathetic tone i

90 SNS catecholamines expand HPCs, which are both targets and s

91 Also, we show that glucocorticoid and catecholamine exposure reorganizes cellular cortical act

92 ion in 46 of 46 patients and most (70%) were catecholamine facilitated.

93 Chromogranin A (CHGA) is coreleased with catecholamines from secretory vesicles in adrenal medull

94 onnectivity and advance our understanding of catecholamine function in the central nervous system.

95 At odds with common understanding of catecholamine function, we found (1) overall reduced int

96 To investigate the interaction between catecholamine functioning and behavioral, and neural res

97 Association of these factors with catecholamine gene variants was tested using single-step

98 iability is predicted by common variation in catecholamine genes and whether it mediates the relation

99 Dbh-/- mice lacking catecholamines had low HPC numbers, reconstituted by ISO

100 fferential role of subcellular mechanisms of catecholamine handling in nerve terminals has not been i

101 Impaired catecholamine handling in the viable infarct border zone

102 1 complexes was accompanied by impairment in catecholamine homeostasis, with significant increases in

103 ngle adrenal chromaffin vesicles filled with catecholamine hormones as they are adsorbed and rupture

104 release functional zone-specific steroid and catecholamine hormones to regulate mammalian stress resp

105 well-documented effect of glucocorticoid and catecholamine hormones, although the underlying mechanis

106 utic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strat

107 This catecholamine imbalance may contribute to the particular

108 shows that chronic elevation in circulating catecholamines in IUGR fetuses persistently inhibits ins

109 (N = 32) that suggests an important role for catecholamines in learning rate regulation.

110 provides opportunity for differentiating the catecholamines in mixtures by monitoring the current at

111 an essential element in the concentration of catecholamines in secretory vesicles.

112 agus nerves that modulates the production of catecholamines in the adrenal glands.

113 ulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation

114 rate-limiting enzyme in the biosynthesis of catecholamines, in the nervous system of Biomphalaria.

115 ciated with the electrochemical oxidation of catecholamines, in which DA and NE have rate constants t

116 a striking convergence and demonstrate that catecholamines increase the precision of neural represen

117 ere, we uncovered a novel mechanism by which catecholamines induce inflammation by increasing prostag

118 Pheochromocytoma is associated with catecholamine-induced cardiac toxicity, but the extent a

119 the driving force behind glucocorticoid- and catecholamine-induced demargination.

120 Here we report that, in vitro, Meto prevents catecholamine-induced down-regulation of S1PR1, a major

121 catecholoestradiol-, 17beta-oestradiol- and catecholamine-induced endothelial cell proliferation may

122 s is strongly related to adipose morphology, catecholamine-induced lipid mobilization (lipolysis), or

123 Deletion of NLRP3 in ageing restored catecholamine-induced lipolysis by downregulating growth

124 Catecholamine-induced lipolysis, the first step in the g

125 signalling mechanisms mediating E2 beta- and catecholamine-induced proliferation.

126 a-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the

127 heart rate was increased; in the presence of catecholamine-induced stress, the frequency of ventricul

128 renergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechan

129 CPVT) are electric diseases characterized by catecholamine-induced ventricular arrhythmias.

130 ght be implemented at a neural level through catecholamine influences on corticostriatal loops.

131 low cardiac output syndrome with need for a catecholamine infusion 48 hours after study drug initiat

132 rdia initiation, termination, sensitivity to catecholamine infusion, and response to adenosine/verapa

133 njury]) who required mechanical ventilation, catecholamine infusion, or both and did not have a poten

134 ence in the composite end point of prolonged catecholamine infusion, use of left ventricular mechanic

135 r pathological conditions induced by chronic catecholamine infusions, BAY reversed both the attenuate

136 During arrhythmia provocation induced by catecholamine injections, TG animals were resistant to t

137 Finally, immunostaining revealed that catecholamine innervation of the dLGN is solely noradren

138 Overproduction of catecholamines is the biochemical hallmark of pheochromo

139 upled beta1-adrenoreceptor (beta1-AR) by the catecholamines isoprenaline (Iso) and adrenaline (Adr) i

140 xycorticosterone acetate-salt, and excessive catecholamines lead to formation of effector like T cell

141 I studies, we examine the effect of baseline catecholamine levels (as indexed by pupil diameter and m

142 CgB); CgA- and CgB-derived peptides regulate catecholamine levels and blood pressure.

143 mic) in LDCV formation and the regulation of catecholamine levels and blood pressure.

144 adrenal LDCV formation and the regulation of catecholamine levels and blood pressure.

145 Gallein also reduced circulating plasma catecholamine levels and catecholamine production in iso

146 as well as a non-linear relationship between catecholamine levels and cognitive functions.

147 ergic activity demonstrated by the increased catecholamine levels and expression of catecholamine bio

148 We pharmacologically increased synaptic catecholamine levels and measured the resulting changes

149 In Study 2 (N = 24), we manipulate catecholamine levels and neural gain using the norepinep

150 ign, we pharmacologically increased synaptic catecholamine levels by administering atomoxetine, an NE

151 tributors to the chronically elevated plasma catecholamine levels observed in HF, where adrenal alpha

152 To replicate the effects of elevated catecholamine levels observed in vivo, cells were treate

153 of the specific impact of these increases in catecholamine levels on perceptual encoding.

154 Baseline catecholamine levels tend to increase with increasing ta

155 idate and amphetamine modulate extracellular catecholamine levels through interaction with dopaminerg

156 When assayed, urinary metanephrine and catecholamine levels were consistently elevated.

157 Urinary catecholamine levels will not be included in response as

158 ed by elevated CB neural activity and plasma catecholamine levels, and elevated reactive oxygen speci

159 Furthermore, catecholamine levels, catecholamine biosynthetic enzymes

160 methods of examining the effect of baseline catecholamine levels, our results show a striking conver

161 c peptide levels, troponin release, elevated catecholamine levels, RV dilatation, and late gadolinium

162 sympathetic adrenal-medullary activation and catecholamine levels, the inflammatory cytokine IL-6, ci

163 c systems and to provide a direct measure of catecholamine levels.

164 es with pupil diameter, an index of baseline catecholamine levels.

165 anges in mRNA transcripts mainly involved in catecholamine metabolism.

166 ssociation between urinary concentrations of catecholamine metabolites (metanephrine and total metane

167 which encodes a protein with homology to the catecholamine methyltransferase COMT that is linked to s

168 Catecholamines modulate the impact of motivational cues

169 Catecholamine murine cultured neurons are more responsiv

170 Hindbrain catecholamine neurons distribute glycemia-related inform

171 al MHC-I can trigger antigenic response, and catecholamine neurons may be particularly susceptible to

172 ing disorder symptoms in response to reduced catecholamine neurotransmission after CD.

173 lations in the gamma range, and modulated by catecholamine neurotransmission.

174 ta, alpha and, beta ranges, and modulated by catecholamine neurotransmission.

175 Dopamine (DA) is one of the most important catecholamine neurotransmitters of the human central ner

176 s the rate-limiting step in the synthesis of catecholamine neurotransmitters, and a reduction in TH a

177 ssible to reduce the interference from other catecholamine neurotransmitters, including L-DOPA, epine

178 Dopamine, one of catecholamine neurotransmitters, plays an important role

179 c susceptibility increases responsiveness to catecholamine neurotransmitters.

180 roxyphenylalanine in the biosynthesis of the catecholamine neurotransmitters.

181 Here, we assessed whether the catecholamine noradrenalin directly modulates the activi

182 nervous system, whose chief effector is the catecholamine norepinephrine (NE).

183 The catecholamine norepinephrine plays a significant role in

184 brain-wide neurophysiological effects of the catecholamines norepinephrine and dopamine on stimulus-e

185 from diverse classes of compounds (peptides, catecholamines, nucleosides, amino acids, etc.).

186 d by polymerization of L-DOPA and endogenous catecholamines on the electrode surface.

187 ric hypoxia, and the intravenous infusion of catecholamines, or absent/decreased, e.g. at rest and in

188 y in freely moving rats to measure real-time catecholamine overflow during acute morphine exposure an

189 It remains unknown whether pro-catecholamine pharmacological agents augment control-rel

190 eficits in schizophrenia would be to use pro-catecholamine pharmacological agents to augment these co

191 gh beta-adrenergic stimulation by endogenous catecholamines plays an important role in lactate produc

192 trols using an amino-acid beverage devoid of catecholamine precursors (tyrosine-phenylalanine depleti

193 oformans requirement of exogenous obligatory catecholamine precursors for melanization to produce iso

194 p28 was 2.7-fold increased by removal of the catecholamine-producing adrenal glands prior to endotoxi

195 ion and identify Nr4a1 as a key regulator of catecholamine production by macrophages.

196 circulating plasma catecholamine levels and catecholamine production in isolated mouse adrenal gland

197 o induce tyrosine hydroxylase expression and catecholamine production, factors required for browning

198 Catecholamines promoted ADRB2-dependent PDAC development

199 Thus, catecholamines reduce intrinsic correlations in a spatia

200 els of spatial organization, indicating that catecholamines reduce the strength of functional interac

201 ous system activation as evidenced by normal catecholamine release and lipolytic activity in response

202 y inhibited nicotinic cholinergic stimulated catecholamine release from chromaffin cells.

203 xocytosis, we next amperometrically analyzed catecholamine release from PC12 cells, revealing that ch

204 re to acute, uncontrollable stress increases catecholamine release in PFC, reducing neuronal firing a

205 edullary axis, which controls stress-induced catecholamine release in support of the fight-or-flight

206 physiological index of outcome-evoked phasic catecholamine release in the cortex-predicted learning r

207 association study for plasma catestatin, the catecholamine release inhibitory peptide derived from ch

208 d by analysis of the fractional detection of catecholamine released between electrodes and exploiting

209 Here, we show that beta-agonists or catecholamines released during intense exercise induce C

210 s been demonstrated as effective in reducing catecholamine requirements in patients with chronic hear

211 the mechanisms linking nutrient overload to catecholamine resistance are poorly understood.

212 t ALK7 signaling contributes to diet-induced catecholamine resistance in adipose tissue, and suggest

213 family receptor ALK7 alleviates diet-induced catecholamine resistance in adipose tissue, thereby redu

214 beta3ARs and Epac1 in a state we define as "catecholamine resistance."

215 rtisol and growth hormone responses, but not catecholamine responses to hypoglycemia.

216 tic tone and responsiveness of adipocytes to catecholamines reveals a novel role for ERbeta in contro

217 II receptor type 1 (AT1R), stimulates acute catecholamine secretion through coupling with the transi

218 umors (pheochromocytoma), gallein attenuated catecholamine secretion, as well as G-protein-coupled re

219 Catecholamines showed reversible or irreversible respons

220 olism and longevity via a cell-nonautonomous catecholamine signal.

221 emia counterregulation modulates insulin and catecholamine signaling and glycogen synthase activity i

222 Dysregulated catecholamine signaling has long been implicated in drug

223 ne, located on chromosome 22q11.2, regulates catecholamine signaling in the prefrontal cortex and is

224 g exposure paired with withdrawal influences catecholamine signaling in vivo.

225 t target in this disorder, and modulation of catecholamine signaling may represent a viable strategy

226 ing the 'inverted U shaped' dose response of catecholamine signaling on cognitive function.

227 In the fasted state, increases in catecholamine signaling promote adipocyte function via t

228 ed during hyperinsulinemic hypoglycemia, and catecholamine signaling via cAMP-dependent protein kinas

229 -regulated in obesity, despite reductions in catecholamine signaling, where it contributes to the dev

230 Although catecholamine signalling in adipocytes is normal in the

231 occurs following inhibition or cessation of catecholamine signalling in IUGR fetuses.

232 hydroxylase-deficient mice (Dbh-/-), lacking catecholamine SNS neurotransmitters, isolated HPCs, and

233 Using a catecholamine-specific neurotoxin and hyperinsulinemic-h

234 The t1/2 of the main catecholamine spike was also increased, consistent with

235 Catecholamines stimulate epithelial proliferation, but t

236 energy storage and adipose expansion, while catecholamines stimulate release of adipose energy store

237 oximately 50%) was associated with abrogated catecholamine-stimulated adiponectin secretion.

238 enhancers and led to a decrease in basal and catecholamine-stimulated expression of brown fat-selecti

239 We report that during catecholamine-stimulated lipolysis, Perilipin 5 is phosp

240 In response to elevated catecholamine stimulation during development of congesti

241 beta-blockers act to block excessive catecholamine stimulation of betaARs to decrease cellula

242 Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overs

243 Furthermore, under catecholamine stimulation, which also increases NO synth

244 able infarct border zone, neuronal vesicular catecholamine storage and protection from metabolic degr

245 lls, CHGA and KLKB1 proteins co-localized in catecholamine storage granules.

246 In contrast, high levels of catecholamines strengthen the primary sensory cortices,

247 Catecholamines such as dopamine increased the fluorescen

248 nd in neuronal presynaptic terminals storing catecholamines such as dopamine.

249 Catecholamines such as epinephrine and norepinephrine pr

250 s the rate-limiting step in the synthesis of catecholamines, such as dopamine, in dopaminergergic neu

251 This catecholamine surge leads, through multiple mechanisms,

252 ic pulmonary vasoconstriction and a profound catecholamine surge occur following WLST that result in

253 hotic drug aripiprazole and the heterocyclic catecholamine surrogates present in the beta2-adrenocept

254 This study demonstrates that catecholamine synapses differentially regulate the exten

255 rosine hydroxylase (TH), a key enzyme in the catecholamine synthesis pathway, and that this activatio

256 hydroxylase (TH; the rate-limiting enzyme in catecholamine synthesis), and serotonin (5HT) to identif

257 expression, the rate-limiting enzyme of the catecholamine synthesis, delineating a mechanism for the

258 cts in diverse cellular processes, including catecholamine synthesis, vasoconstriction, neuronal func

259 ine beta-hydroxylase, an enzyme required for catecholamine synthesis.

260 rotein 2 (MECP2), with known disturbances in catecholamine synthesis.

261 r, the data show that keratinocytes modulate catecholamine synthetic enzymes and release norepinephri

262 ounded and expression levels of the B2AR and catecholamine synthetic enzymes tyrosine hydroxylase and

263 Here, we investigated the keratinocyte catecholamine synthetic pathway in response to acute tra

264 s-evoked cortical responses suggest that the catecholamine systems are well positioned to regulate le

265 ging evidence for a causal role of the human catecholamine systems in learning-rate regulation as a f

266 As the catecholamine systems modulate these cognitive networks,

267 In adipocytes, catecholamines target the beta-adrenergic (beta-AR)/cAMP

268 Dopamine is a catecholamine that acts both as a neurotransmitter and a

269 Dopamine (DA) is a catecholamine that binds to five G protein-coupled recep

270 normal RBCs and SS-RBCs with epinephrine, a catecholamine that binds to the beta-adrenergic receptor

271 Norepinephrine (NE) is a key catecholamine that stimulates contractility by activatin

272 st-cardiac surgery shock requiring high-dose catecholamines, the early HVHF onset for 48 hours, follo

273 me to hemodynamic stabilization, the risk of catecholamine therapy and the duration of such therapy,

274 Bordetella bronchiseptica can use catecholamines to obtain iron from transferrin and lacto

275 ues in a regulatory domain and by binding of catecholamines to the active site.

276 t disease alone, supporting a direct role of catecholamine toxicity that may produce subtle but long-

277 EHM responded to chronic catecholamine toxicity with contractile dysfunction, car

278 through multiple mechanisms, that is, direct catecholamine toxicity, adrenoceptor-mediated damage, ep

279 hypertrophy induced by pressure overload and catecholamine toxicity.

280 Moreover, we investigated the role of catecholamine transmission in these changes by examining

281 s suggest that abstinence-induced changes in catecholamine transmission in visual attention areas (eg

282 MPH enhances catecholamine transmission via blockade of norepinephrin

283 ing transplanted heart, a region with normal catecholamine transport and vesicular storage is surroun

284 ifferences in correlation with expression of catecholamine transporter systems.

285 3)I-MIBG targets cell membrane and vesicular catecholamine transporters of chromaffin cells and facil

286 ncreased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed b

287 y the lipid droplet protein Perilipin 5 as a catecholamine-triggered interaction partner of PGC-1alph

288 elated effects of TBZ were attenuated by the catecholamine uptake inhibitor and antidepressant buprop

289 Regional catecholamine uptake of varying degrees was observed in

290 c degradation are more severely altered than catecholamine uptake.

291 ratory infection experiments determined that catecholamine utilization contributes to the in vivo fit

292 her B. bronchiseptica bfrD nor bfrE imparted catecholamine utilization to B. pertussis.

293 ressure, heart rate, plasma concentration of catecholamines, vasopressin, endothelin, and renin activ

294 hrome b561 (CYB561), the electron shuttle in catecholamine vesicle membranes for transmitter biosynth

295 atecholoestradiols, to 17beta-oestradiol and catecholamines, we observed that convergent MAPKs signal

296 ic signaling in MCF-7 cells, indicating that catecholamines were the responsible exercise factors.

297 Three different carbon-11-labeled catecholamines were used for positron emission tomograph

298 thetic nervous system induces the release of catecholamines, which activate beta-adrenergic receptors

299 exposure results in the systemic release of catecholamines, which engage the beta2-adrenergic recept

300 supports the disproportionation reaction of catecholamines, which has been previously reported, but