NorepinephrineNorepinephrine
MedChemExpress (MCE)
HY-13715
51-41-2
Levarterenol
L-Noradrenaline
99.43%
4°C, protect from light, stored under nitrogen *In solvent : -80°C, 6 months
-20°C, 1 month (protect from light, stored under nitrogen)
Room temperature in continental US
may vary elsewhere.
Norepinephrine (Levarterenol
L-Noradrenaline) is a potent adrenergic receptor (AR) agonist. Norepinephrine activates α1, α2, β1 receptors.
Norepinephrine (NE) is generally considered to be a β1-subtype selective adrenergic agonist over β2-adrenoceptor. Norepinephrine(NE) also has direct activity at the β2-adrenoceptor in higher concentrations[1]. Adipocytes from the inguinal fat pad (iWA) or the interscapular fat pad (BA) are isolated from neonatal wild-type C57BL/6J mice and cultured. To examine the effect of activating AT2 upon β-adrenergic signaling, cAMP production is first assessed in response to Norepinephrine (NE, 10 μM) with or without CGP (10 nM) co-treatment.Norepinephrine (NE) increases cAMP as expected in iWA, and CGP does not alter this effectNorepinephrine (NE) is also known to induce lipolysis, and liberated fatty acids are required to functionally activate UCP1 protein and to stimulate heat production. CREB phosphorylation at Ser133 is increased after Norepinephrine (NE) treatment and significantly attenuated with CGP co-treatment in mouse iWA[3].
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} Induction of cardiomyopathy[5][6] Background Norepinephrine is a potent growth factor for cardiomyocytes, and long-term infusion of sub-hypertensive doses of Norepinephrine in animals can cause an increase in myocardial mass and left ventricular wall thickness. Norepinephrine activates the raf-1 kinase/MAP kinase cascade through α1 and β-adrenergic stimulation, and the signaling pathways from these two receptors work synergistically to induce cardiomyocyte hypertrophy. Specific Mmodeling Methods Rat: Spragues-Dawley rats • adult (6 months old) • Male &bull.Administration: Each rat was continuously injected with 100 μg/kg/h or 200 μg/kg/h through an osmotic minipump. Note Modeling Record Molecular changes: Significantly increased Dnmt activity and the expressions of Dnmt1, 3a, and 3b in the left ventricle.Significantly increased the mRNA expressions of fetal genes ANP, BNP, and βMHC in the left ventricle.Significantly increased ROS production in the left ventricle and increased global genomic DNA methylation and gene-specific CpG methylation at the Egr-1 binding site of the left ventricular PKCε promoter region in a concentration-dependent manner.Increased lactate dehydrogenase release in a concentration-dependent manner.Significantly reduced the left ventricular developed pressure and dP/dtmax, inducing the upregulation of myotrophin and downregulation of four-and-a-half LIM domains protein 2 (FHL2).Phenotype observations: Increased the myocardial infarction area and sustained the elevation of blood pressure.Induced cardiac hypertrophy and reduced cardiac contractility.Increased the left ventricular weight. Correlated Product(s): 5-Aza-2’-deoxycytidine (HY-A0004), Prazosin (HY-B0193), Propranolol (HY-B0573B)
Subcutaneous preadipocytes derived from a 38-year old non-diabetic female donor are immortalized with TERT and HPV E6/E7. For the current studies, a stable diploid clone (referred to as clone B) with consistent differentiation capacity is isolated by ring cloning. Cells are grown in preadipocyte PGM2 media. Once cells are confluent, differentiation is induced by incubation in differentiation media consisting of dexamethasone, IBMX, indomethacin, and additional insulin. Cells are differentiated for 10 days. Prior to treatment, media is replaced with PGM2 media for one day and then switched to serum-free media overnight for treatments. Adipocytes are treated for 6 hours with vehicle, Norepinephrine (NE, 10 μM), CGP (10 nM), or Norepinephrine (NE) and CGP[2].
α1-adrenergic receptor α2-adrenergic receptor Beta-1 adrenergic receptor Microbial Metabolite Human Endogenous Metabolite
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[1]. Brian P Ramos, et al. Adrenergic pharmacology and cognition: focus on the prefrontal cortex. Pharmacol Ther. 2007 Mar
113(3):523-36. [Content Brief]
[2]. MacGregor DA, et al. Relative efficacy and potency of beta-adrenoceptor agonists for generating cAMP in human lymphocytes. Chest. 1996 Jan
109(1):194-200. [Content Brief]
[3]. Littlejohn NK, et al. Suppression of Resting Metabolism by the Angiotensin AT2 Receptor. Cell Rep. 2016 Aug 9
16(6):1548-60. [Content Brief]
[4]. Xinyu Xu, et al. Binding pathway determines norepinephrine selectivity for the human β 1 AR over β 2 AR. Cell Res. 2021 May
31(5):569-579. [Content Brief]
[5]. Xiao D, et al. "Inhibition of DNA methylation reverses norepinephrine-induced cardiac hypertrophy in rats." Cardiovascular research 101.3 (2014): 373-382. [Content Brief]
[6]. Yamazaki, et al. "Norepinephrine induces the raf-1 kinase/mitogen-activated protein kinase cascade through both α1-and β-adrenoceptors." Circulation 95.5 (1997): 1260-1268.
