Norepinephrine hydrochlorideCAS# 329-56-6 |
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Quality Control & MSDS
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| Cas No. | 329-56-6 | SDF | Download SDF |
| PubChem ID | 11672905 | Appearance | Powder |
| Formula | C8H12ClNO3 | M.Wt | 205.64 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Noradrenaline hydrochloride | ||
| Solubility | Soluble in DMSO | ||
| Chemical Name | 4-[(1R)-2-amino-1-hydroxyethyl]benzene-1,2-diol;hydrochloride | ||
| SMILES | C1=CC(=C(C=C1C(CN)O)O)O.Cl | ||
| Standard InChIKey | FQTFHMSZCSUVEU-QRPNPIFTSA-N | ||
| Standard InChI | InChI=1S/C8H11NO3.ClH/c9-4-8(12)5-1-2-6(10)7(11)3-5;/h1-3,8,10-12H,4,9H2;1H/t8-;/m0./s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Norepinephrine hydrochloride is a β1-selective adrenergic receptor agonist with EC50 of 5.37 μM.In Vitro:Norepinephrine (NE) bitartrate monohydrate is generally considered to be a β1-subtype selective adrenergic agonist. 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 effect. Norepinephrine (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[2]. References: | |||||
Norepinephrine hydrochloride Dilution Calculator
Norepinephrine hydrochloride Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 4.8629 mL | 24.3143 mL | 48.6287 mL | 97.2573 mL | 121.5717 mL |
| 5 mM | 0.9726 mL | 4.8629 mL | 9.7257 mL | 19.4515 mL | 24.3143 mL |
| 10 mM | 0.4863 mL | 2.4314 mL | 4.8629 mL | 9.7257 mL | 12.1572 mL |
| 50 mM | 0.0973 mL | 0.4863 mL | 0.9726 mL | 1.9451 mL | 2.4314 mL |
| 100 mM | 0.0486 mL | 0.2431 mL | 0.4863 mL | 0.9726 mL | 1.2157 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Norepinephrine is a catecholamine with multiple roles including those as a hormone and a neurotransmitter.
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[Effects of benidipine hydrochloride (Coniel) on blood pressure, heart rate and plasma norepinephrine concentration in spontaneously hypertensive rats].[Pubmed:10480159]
Nihon Yakurigaku Zasshi. 1999 May;113(5):317-26.
We investigated the effects of benidipine hydrochloride (benidipine, Coniel) on blood pressure, heart rate and plasma norepinephrine (NE) concentration in spontaneously hypertensive rats and compared them with those of other calcium channel blockers. Benidipine (2 mg/kg, p.o.) was compared with the equihypotensive doses of nifedipine (5 mg/kg), cilnidipine (6 mg/kg) and amlodipine (3 mg/kg). All the 4 calcium channel blockers exhibited significant antihypertensive effects. Nifedipine and cilinidipine significantly increased heart rate, as compared with that in the control group, whereas benidipine or amlodipine did not significantly affect it. The area under the curves for hypotensive effect and tachycardic effect for 10 hr after the drug administration were compared among the 4 compounds. As a result, the tachycardic effect of benidipine was significantly lower than those of nifedipine, cilnidipine and amlodipine, while the hypotensive effects were similar among the 4 compounds. Nifedipine and amlodipine, significantly increased plasma NE concentration, cilnidipine tended to increase it. In contrast, benidipine did not significantly affect plasma NE concentration. These results suggest that the effects of benidipine on plasma NE concentration and heart rate are less prominent than those of the other calcium channel blockers.
Verification of protector effect of the norepinephrine and felypressin upon the cardiovascular system under action of the lidocaine hydrochloride and prilocaine hydrochloride in anesthetized rats.[Pubmed:12220948]
Pharmacol Res. 2002 Aug;46(2):107-11.
Vasoconstrictor substances, as norepinephrine and epinephrine, were mixtured to local anesthetics to decrease their toxic effects and to prolong the depth of the anesthesia. However, these catecholamines produce systolic and diastolic hypertension. The effects of felypressin, a synthetic vasoconstrictor, upon arterial blood pressure and heart are lesser than those of norepinephrine or epinephrine, but due to its effects like oxytocin these catecholamines are yet the most used vasoconstrictors in association with lidocaine or another anesthetic salt. These vasoconstrictors are contraindicated for some physician, mainly for cardiac patients. But, are the catecholamines or is the salt the most dangerous components of the local anesthetic? The effects of the salt and catecholamines are opposite, but which of these exercises their effects first when inside blood vessel? Singi et al. [Pharmacol. Res. 44 (2001)] demonstrated that the first effect is always of the salt and that norepinephrine promotes protector effects upon guinea-pig isolated heart against lidocaine action. But, is this true for in vivo animals? The present study was performed with the aiming to answer this question and to verify if felypressin can induce the same effect of the norepinephrine. Fourteen Rattus norvegicus albinus, weighing 350g on average, were used. After being anesthetized with sodic thiopental, they were tracheostomizeds and one jugular and one carotid were cannuled for application of substances and to record the blood arterial pressure, respectively. The ECG was gotten through electrodes located in the front and back paws of the animals. The animals were separated in two groups, each one with seven rats. The lidocaine hydrochloride 2% in the doses of 600 microg and 3% in the doses of 900 microg acted on the cardiovascular system reducing the arterial pressure and modifying the electrocardiogram, while the prilocaine hydrochloride, in the same doses, also reduced the arterial pressure, but did not modify the electrocardiogram. When norepinephrine was associated to lidocaine 3% hydrochloride, it was possible to observe that this salt always exercised its effect first and a protective effect against the fall of pressure produced for the lidocaine. The same protective effect did not occur when felypressin was associated with prilocaine hydrochloride 3%.
[Effects of tramadol hydrochloride preconditioning on the activation of nuclear factor-KappaB induced by norepinephrine in cultured neonatal rat cardiomyocytes].[Pubmed:24225208]
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Nov;25(11):646-9.
OBJECTIVE: To investigate the effects of tramadol hydrochloride preconditioning on activation of nuclear factor-KappaB (NF-KappaB) induced by norepinephrine (NE) in cultured neonatal rat cardiomyocytes. METHODS: 1 to 3-day old Sprague-Dawley (SD) rats were raised, and their cardiomyocytes were cultured for 4 to 5 days. Sixteen wells of cultured cardiomyocytes were randomly divided into four groups (n=4): blank control group, NE1 group in which the cells were incubated with 1x10(-6) mmol/L of NE, NE2 group in which cells were incubated with 1x10(-7) mmol/L of NE, and NE3 group in which cells were incubated with 1x10(-8) mmol/L of NE. Another 12 wells of cultured cardiomyocytes were randomly divided into three groups (n=4): blank control group, NE3 group in which cells were incubated with 1x10(-8) mmol/L of NE, tramadol plus NE group (T + NE group) in which cells were incubated with 1x10(-5) mmol/L of tramadol hydrochloride plus 1x10(-8) mmol/L of NE. Tramadol hydrochloride was added 30 minutes before the use of NE in T + NE group. After exposure to NE for 24 hours, the expression and activation of NF-KappaB in the cultured cardiomyocytes were determined by immunocytochemistry and flow cytometry (FCM). RESULTS: The results of immunocytochemistry showed that the expression of NF-KappaB (including average optical density and positive units) in NE3 group was significantly increased as compared with that in the blank control group (A average optical density: 0.30+/-0.03 vs. 0.12+/-0.04, t=7.200, P=0.008; positive units: 39+/-14 vs. 22+/-6, t=4.610, P=0.020). The results of FCM showed that the levels of cytoplasm NF-KappaB in cultured cardiomyocytes were decreased significantly in NE1 group, NE2 group and NE3 group compared with blank control group [(45.8+/-1.9)%, (38.3+/-1.8)%, (20.9+/-1.6)% vs. (54.6+/-0.6)%, all P<0.05], and the level in NE3 group was significantly lower than that in NE1 and NE2 groups (both P<0.05). The level of the cardiomyocytes cytoplasm NF-KappaB in T + NE group was higher than that in NE3 group [(57.8+/-0.4)% vs. (20.9+/-1.6)%, t=57.524, P=0.001]. CONCLUSIONS: Tramadol hydrochloride preconditioning can inhibit the activation of NF-KappaB induced by NE in cultured rat cardiomyocytes. It plays a protective role in ischemia myocardium at cell level.
(-)-(1R,2R)-3-(3-dimethylamino-1-ethyl-2-methyl-propyl)-phenol hydrochloride (tapentadol HCl): a novel mu-opioid receptor agonist/norepinephrine reuptake inhibitor with broad-spectrum analgesic properties.[Pubmed:17656655]
J Pharmacol Exp Ther. 2007 Oct;323(1):265-76.
(-)-(1R,2R)-3-(3-dimethylamino-1-ethyl-2-methyl-propyl)-phenol hydrochloride (tapentadol HCl) is a novel micro-opioid receptor (MOR) agonist (Ki = 0.1 microM; relative efficacy compared with morphine 88% in a [35S]guanosine 5'-3-O-(thio)triphosphate binding assay) and NE reuptake inhibitor (Ki = 0.5 microM for synaptosomal reuptake inhibition). In vivo intracerebral microdialysis showed that tapentadol, in contrast to morphine, produces large increases in extracellular levels of NE (+450% at 10 mg/kg i.p.). Tapentadol exhibited analgesic effects in a wide range of animal models of acute and chronic pain [hot plate, tail-flick, writhing, Randall-Selitto, mustard oil colitis, chronic constriction injury (CCI), and spinal nerve ligation (SNL)], with ED50 values ranging from 8.2 to 13 mg/kg after i.p. administration in rats. Despite a 50-fold lower binding affinity to MOR, the analgesic potency of tapentadol was only two to three times lower than that of morphine, suggesting that the dual mode of action of tapentadol may result in an opiate-sparing effect. A role of NE in the analgesic efficacy of tapentadol was directly demonstrated in the SNL model, where the analgesic effect of tapentadol was strongly reduced by the alpha2-adrenoceptor antagonist yohimbine but only moderately attenuated by the MOR antagonist naloxone, whereas the opposite was seen for morphine. Tolerance development to the analgesic effect of tapentadol in the CCI model was twice as slow as that of morphine. It is suggested that the broad analgesic profile of tapentadol and its relative resistance to tolerance development may be due to a dual mode of action consisting of both MOR activation and NE reuptake inhibition.
