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Norepinephrine

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Norepinephrine is a laboratory product produced by Merck Group. It is a neurotransmitter and hormone that plays a role in the sympathetic nervous system. The core function of Norepinephrine is to regulate physiological processes such as heart rate, blood pressure, and pupil dilation.

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Lab products found in correlation

Claycomb medium, by Merck Group (44 mentions) L glutamine, by Merck Group (32 mentions) L glutamine, by Thermo Fisher Scientific (32 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (30 mentions) Fetal bovine serum (fbs), by Merck Group (29 mentions) Epinephrine, by Merck Group (28 mentions) Dopamine, by Merck Group (20 mentions) Fibronectin, by Merck Group (20 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (19 mentions) Acetylcholine, by Merck Group (17 mentions) Gelatin, by Merck Group (16 mentions) Propranolol, by Merck Group (16 mentions) Penicillin streptomycin, by Merck Group (16 mentions) Penicillin, by Thermo Fisher Scientific (16 mentions) Streptomycin, by Thermo Fisher Scientific (14 mentions) Isoproterenol, by Merck Group (12 mentions) Phenylephrine, by Merck Group (12 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (10 mentions) Serotonin, by Merck Group (9 mentions) Glutamax, by Thermo Fisher Scientific (9 mentions)

Close spelling variants of this product

Norepinephrine [( ±)-Arterenol] L-norepinephrine Norepinephrine bitartrate salt monohydrate (NE; DL-norepinephrine hydrochloride Norepinephrine bitartrate L-(−)-norepinephrine (+)-bitartrate salt monohydrate L-norepinephrine hydrochloride Dexamethasone (D4902), insulin (I5500), 3-IsoButyl-1-MethylXanthine (IBMX, I7018), biotin (B4639), D-pantothenic acid hemicalcium salt (P5155), isoproterenol (I6504), CL-316,243 (C5976), norepinephrine (A7257), dibutyryl-cAMP (D0260), triiodothyronine (T5516), acetylcholine chloride (A2661), nicotine (N3876), L-(−)-norepinephrine (+)-bitartrate salt monohydrate (NE, Norepinephrine bitartrate salt monohydrate

248 protocols using norepinephrine

1

Oxytocin Modulation of IL-6 Secretion in Ovarian Cancer

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To evaluate the effects of oxytocin on interleukin-6 secretion, ovarian tumor cells were incubated with oxytocin (Bachem, Torrance, CA) for six hours under basal or norepinephrine-stimulated conditions. norepinephrine stimulation was used to enhance an inflammatory challenge as norepinephrine has been demonstrated to enhance interleukin-6 secretion by ovarian tumor cells (Nilsson et al., 2007 (link)). In the norepinephrine-stimulated conditions, ovarian tumor cells were concurrently incubated with 10 μM norepinephrine (Sigma, St. Louis, MO) with or without 1 nM oxytocin for 6 hours. The oxytocin dose of 1 nM was chosen because it is near the Kd of the ligand binding to the oxytocin receptor (Gimpl and Fahrenholz, 2001 (link)) and it was also in the upper range of oxytocin detected in clinical samples of patients’ ascites fluid. To evaluate the specificity of the oxytocin response, HEYA8 and SKOV-3 cells were incubated with 10 nM of Atosiban (cat. No. A3480, Sigma-Millipore, St. Louis, MO), an oxytocin receptor antagonist, during a six hour incubation in the presence of 10 μM norepinephrine and with or without 1 nM oxytocin.
Cuneo M.G., Szeto A., Schrepf A., Kinner E.M., Schachner B.I., Ahmed R., Thaker P.H., Goodheart M., Bender D., Cole S.W., McCabe P.M., Sood A.K., Lutgendorf S.K, & Mendez A.J. (2019). Oxytocin in the tumor microenvironment is associated with lower inflammation and longer survival in advanced epithelial ovarian cancer patients. Psychoneuroendocrinology, 106, 244-251.
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2

Evaluation of Vasorelaxation Responses

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Endothelium-dependent vasorelaxation was measured in response to ACh following 20-minute incubation with 5 μL 10−3 M norepinephrine (Sigma-Aldrich, St. Louis, MO, USA).17 (link) ACh (Sigma-Aldrich) was added every one minute in steadily increasing doses from 10−11 M to 3×10−5 M well concentration. The vessels were then washed three times with PSS over 10 minutes, and the resting tension was readjusted to 36 mN. Vessels were again incubated with 10-3 M norepinephrine for 20 minutes, and endothelium-independent vasorelaxation was measured in response to escalating doses of SNP (Sigma-Aldrich) from 10−11 M to 3×10−5 M. The vessels were then washed three times with PSS over 10 minutes, and the resting tension was readjusted again to 36 mN. After 20 minutes of incubation with norepinephrine, we measured the response to the heme-independent soluble guanylyl cyclase activator cinaciguat (Sigma-Aldrich), using a dose range from 10−20 M to 10−9 M.16 (link)
Mace E.H., Kimlinger M.J., No T.J., Dikalov S.I., Hennessy C., Shotwell M.S., Billings FT I.V, & Lopez M.G. (2022). Soluble guanylyl cyclase activation rescues hyperoxia-induced dysfunction of vascular relaxation. Shock (Augusta, Ga.), 58(4), 280-286.
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3

GC Cell Line Treatment and Analysis

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The SGC-7901 and BGC-823 human GC cell lines were purchased from the Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences (Shanghai China), and were incubated in RPMI-1640 (Gibco; Thermo Fisher Scientific, Inc., Waltham, MA, USA) supplemented with 10% FBS (Gibco; Thermo Fisher Scientific, Inc.). All cell lines were grown in a humidified chamber supplemented with 5% CO2 at 37°C. Norepinephrine (10 µM; Sigma, Shanghai, China), 5 µM terbutaline (Sigma), 1 µM xamoterol (Tocris Chemicals, Shanghai, China), 10 µM propranolol (Sigma), 50 nMH 89 2HCL (Selleck Chemicals, Shanghai, China), 5 µM Chloroquine (Selleck Chemicals) in PBS were used to treat the cells for 24 h prior to testing. In addition, 5 µg/ml E64d (Sigma) and 5 µg/ml pepstain A (Sigma) were used to treat the cells following Norepinephrine treatment.
Zhi X., Li B., Li Z., Zhang J., Yu J., Zhang L, & Xu Z. (2019). Adrenergic modulation of AMPK-dependent autophagy by chronic stress enhances cell proliferation and survival in gastric cancer. International Journal of Oncology, 54(5), 1625-1638.
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4

Zebrafish Embryonic Pharmacological Interventions

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Camptothecin (Sigma # C9911) treatment was performed according to a previously described method [45] (link) with modifications. The compound (60 µM in 0.1% dimethyl sulfoxide [DMSO]) was applied to 48 hpf embryos, which were harvested at 57 hpf for the 3β-Hsd activity assay. The treatment of embryos with 2,3-butanedione 2-monoxime (2,3-BDM; Sigma #B0753) was as described in an earlier report [46] (link), except that dechorionated embryos were immersed in various concentrations of 2,3-BDM starting from 1.5 dpf. Norepinephrine treatment was performed by treating dechorionated embryos with 0.01, 0.1 or 1 mM Norepinephrine (Sigma A7257) freshly prepared in egg water. L-NAME treatment was performed by treating dechorionated embryos with freshly prepared 100 µM Nω-nitro-l-arginine methyl ester (l-NAME) (#N5751, Sigma) in egg water with 0.1% DMSO at 36 hpf. For l-arginyl-l-glycyl-l-aspartic acid (RGD; #G1269, Sigma) treatment, the peptide was reconstituted to 1 mM in filter-sterilized egg water and applied to dechorionated embryos at a final concentration of 100 µM at 26 hpf; embryos were collected at 2.5 dpf and fixed for histological assays.
Chou C.W., Zhuo Y.L., Jiang Z.Y, & Liu Y.W. (2014). The Hemodynamically-Regulated Vascular Microenvironment Promotes Migration of the Steroidogenic Tissue during Its Interaction with Chromaffin Cells in the Zebrafish Embryo. PLoS ONE, 9(9), e107997.
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5

Cardiac Myocyte Imaging: HL-1 Cell Protocol

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HL-1 cardiac myocytes (provided by Dr. William Claycomb, Lousiana State University Health Science Center, New Orleans, LA, USA), which are phenotypically similar to mature cardiomyocytes and exhibit spontaneous depolarization[11 (link)], were used as an in vitro cellular imaging target. HL-1 cells passages 60–80 were maintained in Claycomb medium (Sigma-Aldrich Inc., St. Louis, MO, USA) with 10% fetal bovine serum (Sigma-Aldrich Inc., St. Louis, MO, USA, Lot# 12J001), 1% Penicillin/Streptomycin (Invitrogen), 1% Glutamax (Invitrogen), and 0.1 mM Norepinephrine (Sigma-Aldrich Inc., St. Louis, MO, USA). Cells were subcultured (1:3) every 4 days[12 (link)]. 12 hours before imaging, HL-1 cells were seeded at 80,000 cells/cm2 in Nunc™ Lab-Tek™ II CC2™ two chamber slides (Thermo Fisher Scientific, Inc., Waltham, MA, USA). Just prior to imaging, cells were rinsed three times and incubated for 20 minutes in Tyrode’s solution[13 ] containing 0.1 mM Norepinephrine, 200 μM Asz and 10 μM DMSO (Sigma-Aldrich Inc., St. Louis, MO, USA, to improve cellular uptake of Asz). Cells were then thrice rinsed with Tyrode’s solution containing Norepinephrine and immediately imaged using either optical or photoacoustic imaging.
Dana N., Fowler R.A., Allen A., Zoldan J., Suggs L, & Emelianov S. (2016). In vitro photoacoustic sensing of calcium dynamics with Arsenazo III. Laser physics letters, 13(7), 075603.
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6

Vascular Reactivity Assessment Protocol

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After viability assessment with KPSS, each vessel was stimulated as follows: (1) Cumulative addition of norepinephrine (Sigma‐Aldrich), 10−9, 3×10−9, 10−8, 3×10−8, 10−7, 3×10−7, 10−6, 3×10−6, 10−5 mol/L with 3 to 5 minutes incubation per concentration. (2) Endothelial function was assessed via the cumulative response to acetylcholine (Sigma‐Aldrich) achieved by adding serial concentrations (mol/L) 10−9, 3×10−9, 10−8, 3×10−8, 10−7, 3×10−7, 10−6, 3×10−6, 10−5 to a preconstricted vessel with 10−5 norepinephrine. After 1 hour of incubation with 5×10−5 mol/L NG‐monomethyl‐l‐arginine (Sigma), a NO synthase inhibitor, the responses to acetylcholine were repeated as in step 2 above.
Khavandi K., Aghamohammadzadeh R., Luckie M., Brownrigg J., Alam U., Khattar R., Malik R.A., Heagerty A.M, & Greenstein A.S. (2017). Abnormal Remodeling of Subcutaneous Small Arteries Is Associated With Early Diastolic Impairment in Metabolic Syndrome. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 6(4), e004603.
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7

Maintenance of HL1 Cardiac Cells

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HL1 cells were maintained according to published methods [15 (link)]. Briefly, cells were plated in T25 flasks coated with 25μg fibronectin (Sigma-Aldrich, F1141) in 2 mL 0.02% bovine gelatin (Sigma-Aldrich, G9391) in water. Cells were maintained in Claycomb Medium (Sigma-Aldrich, 51800C) supplemented with 10% FBS (Sigma-Aldrich, F2442, Batch 11A568, US origin), 100 μg/mL Penicillin-Streptomycin (Sigma-Aldrich, P4333), 0.1mM norepinephrine (Sigma-Aldrich, A0937), and 2mM L-glutamine (Sigma-Aldrich, G7513). norepinephrine stock (10mM) was made up in 30mM ascorbic acid (Sigma-Aldrich, A7506) and filtered using a 0.2um syringe filter (Gelman Sciences, 4192). Cells were grown at 37°C in 5% CO2 and were passaged upon reaching confluence every 2–3 days by dissociating into single cells using 0.05% Trypsin in 0.02% EDTA-Na (Sigma-Aldrich, T3924).
Ramachandran S., Lowenthal A., Ritner C., Lowenthal S, & Bernstein H.S. (2017). Plasma microvesicle analysis identifies microRNA 129-5p as a biomarker of heart failure in univentricular heart disease. PLoS ONE, 12(8), e0183624.
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8

Pharmacological Dissection of Norepinephrine Signaling

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For the norepinephrine study, we selectively blocked each receptor subtype with yohimbine, phentolamine, prazosin (each 10 μM, from Sigma-Aldrich) or propranolol (10 μM, from Merck Millipore) 30 min before stimulation with norepinephrine (1 μM, from Sigma-Aldrich). For the pathway study, LY294002 (PI3K inhibitor, Cell Signaling Technology, 50 μM) or SB203580 (p38 inhibitor, Merck Millipore, 10 μM) was added 1 hour before simulation with the cocktail, and H89 (PKA inhibitor, Sigma-Aldrich, 10 μM), KN-93 (CAMKII inhibitor, Sigma-Aldrich, 0.5 μM), JNK inhibitor II (Merck Millipore, 10 μM), U0126 (ERK1/2 inhibitor, Cell Signaling Technology, 10 μM), Latrunculin B (actin polymerization inhibitor, Merck Millipore, 0.3μM), or Rho kinase Inhibitor (Merck Millipore, 100nM) was added 30 min before stimulation.
Mikhail C., Vaucher A., Jimenez S, & Tafti M. (2017). ERK signaling pathway regulates sleep duration through activity-induced gene expression during wakefulness. Science signaling, 10(463).
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9

Aortic Relaxation Measurement Protocol

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Endothelium-dependent vasorelaxation to acetylcholine or endothelium-independent relaxation to sodium nitroprusside was determined using an organ bath chamber (DMT Inc., Denmark) as previously described (Cai et al., 2020 (link)). The thoracic aorta was cut into 3-mm aortic rings, and the aortic rings were contracted twice with KPSS solution containing 60 mmol/L KCL. The rings were precontracted to 70% of maximal constriction force to norepinephrine (about 30 nmol/L norepinephrine, Sigma-Aldrich, St. Louis, MO). After the contraction reached a plateau, an accumulative dose of acetylcholine (10–9 to 10–5 mol/L, Sigma-Aldrich, St. Louis, MO) or sodium nitroprusside (10–9 to 10–5 mol/L, Sigma-Aldrich) was added in the organ chamber, and maximal response to an agonist (Emax) and the concentration of agonist required for a half-maximal response curve (ED50) were determined and calculated from the concentration-response curve, using best fit to a logistic sigmoid function.
Yang X.F., Wang H., Huang Y., Huang J.H., Ren H.L., Xu Q., Su X.M., Wang A.M., Ren F, & Zhou M.S. (2022). Myeloid Angiotensin II Type 1 Receptor Mediates Macrophage Polarization and Promotes Vascular Injury in DOCA/Salt Hypertensive Mice. Frontiers in Pharmacology, 13, 879693.
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10

Electrophysiological Assessment of Cardiomyocytes on MEAs

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Electrical activity of the human cardiomyocytes plated on patterned MEAs was recorded following 4–10 days in vitro (DIV) using a Multichannel Systems 60 channel amplifier (MEA 1040, Multichanel Systems). Prior to recording, the cells were allowed to equilibrate for 15 min in the lab atmosphere at 37°C. Temperature was maintained with a TC02 temperature controller (Multichannel Systems). The cells were stimulated using a STG 1002 stimulator (Multichannel Systems) by applying 1 ms wide bipolar square pulses of 500–700 mV amplitude at increasing frequencies ranging from 0.5 Hz to 2.5 Hz in 0.5 Hz increments. The recording medium was the same as the plating medium. For drug experiments, sotalol, (Sigma, cat#S0278), norepinephrine (Sigma, cat#A7257) or verapamil (Sigma, cat#381195) were added to the bathing medium in increasing concentrations of 10, 30, 100 and 300 μM – sotalol, 0.1, 0.3, 1 and 3 μM – norepinephrine, and 0.3, 1, 3 and 10 μM – verapamil. In all drug experiments, for control and each new drug concentration a total of 5 minutes of recordings were performed, the first 150 seconds with no stimulation, followed by 30 seconds of stimulation, and ended with no stimulation. The data was converted to pClamp (Axon Instruments) format using MC-Data Tool (Multichannel Systems) and analyzed with Clampfit (Axon Instruments) software and software written in Matlab.
Stancescu M., Molnar P., McAleer C.W., McLamb W., Long C.J., Oleaga C., Prot J.M, & Hickman J.J. (2015). A phenotypic in vitro model for the main determinants of human whole heart function. Biomaterials, 60, 20-30.
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