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Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
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Accessible (Haz class 3, 4, 5 or 8), International
Nitric oxide synthase (NOS) is an enzyme responsible for the production of nitric oxide (NO) from L-arginine. L-NAME HCl is an inhibitor for bovine brain NOS and mouse macrophage NOS with Ki values of 15 nM and 4.4 μM, respectively[1]. In rMC-1 cells, the accumulation of NO induced by glucose (25 mM) was inhibited by 1 mM L-NAME HCl. The treatment of L-NAME HCl at 1 mM also led to significantly decreased cell death in glucose-stimulated rMC-1 cells. Elevated production of PGE2 in BREC cells was significantly suppressed by 1 mM L-NAME HCl[2]. With the presence of 30 μM L-arginine and 100 μM NADPH, L-NAME HCl at 0.1 – 100 μM dose-dependently inhibited the formation of cyclic GMP in endothelial cytosol with an IC50 value of 3.1 μM. It also inhibited [3H]-citrulline formation with an IC50 value of 0.09 μM. L-NAME HCl at 0.1 – 300 μM induced endothelium-dependent contraction of rings of rat aorta with an EC50 value of 26 μM in the presence of 10 nM phenylephrine. The relaxation of rings of rat aorta was inhibited by 0.1 – 10 μM L-NAME HCl at a dose-dependent manner with an IC50 value of 0.54 μM. In Wistar rats, i.v. administration of L-NAME HCl (0.03 – 300 mg/kg) dose-dependently increased the mean arterial blood pressure with an EC50 value of 2.4 mg/kg, and the highest blood pressure induced by L-NAME HCl was 44.1 mmHg. The same treatment of L-NAME HCl also resulted in bradycardia at a concentration-dependent manner[3].
作用机制
L-NAME HCl is a soluble methyl ester that inhibits NOS. Intracellular esterases convert a variable and unknown fraction of L-NAME to L-NNA, which tightly but reversibly binds to NOS, competing with L-arginine[4].
H-Arg(NO2)-OMe·HCl 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Human umbilical vascular endothelial cells (HUVECs)
1 mM
4 days
To induce endothelial-to-mesenchymal transition (EndoMT) and study its reversibility. Results showed that the combination of L-NAME and Ang II can stimulate EndoMT in HUVECs, and this process can be reversed.
Front Pharmacol. 2022 Jun 23;13:912660.
mouse aortic segments
300 µM
20 min
To evaluate the involvement of the endothelial cell layer in regulating VSMC contraction and tone, L-NAME inhibits NO production, further increasing contraction.
Int J Mol Sci. 2021 Nov 26;22(23):12812.
Fetal vessels
100 μM
In fetal vessels, L-NAME was used along with ODQ and INDO to study ACh-induced vasodilation. Results showed that ACh-induced relaxation was significantly reduced in SD fetal vessels.
Sci Rep. 2015 May 8;5:9753.
Weanling vessels
100 μM
In weanling vessels, L-NAME was used along with ODQ and INDO to study ACh-induced vasodilation. Results showed that ACh-induced relaxation was significantly reduced in SD weanling vessels.
Sci Rep. 2015 May 8;5:9753.
Adult vessels
100 μM
In adult vessels, L-NAME was used along with ODQ and INDO to study ACh-induced vasodilation. Results showed that ACh-induced relaxation was significantly reduced in SD adult vessels.
Sci Rep. 2015 May 8;5:9753.
H-Arg(NO2)-OMe·HCl 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
Gastric emptying model
Intraperitoneal injection
50 mg/kg
Single dose
L-NAME significantly delayed gastric emptying, while L-Arginine was not directly used in the experiment.
Gut. 2005 Aug;54(8):1078-84
Mice
Hypertension model
Oral
0.5mg/mL
2 weeks L-NAME, 3 weeks high salt diet
To study the role of CD70 and immunological memory in hypertension
Circ Res. 2016 Apr 15;118(8):1233-43
Mice
ACE 10/10 and ACE 3/3 mice
Drinking water
0.5 mg/mL for WT mice, 1.5 mg/mL for mutant mice
4 weeks of L-NAME, 1-week washout, 3 weeks of high salt diet
To study the development of salt sensitivity following renal injury, results showed that mice lacking renal ACE did not develop hypertension after high salt diet
To investigate the role of EP3 receptors in salt-sensitive hypertension, results showed that EP3 receptor deficient mice had significantly attenuated blood pressure elevation and renal inflammation during the salt-feeding phase.
To study the role of SGK1 in CD11c+ antigen-presenting cells, finding that SGK1 deletion attenuates salt-sensitive hypertension and renal inflammation.
Hypertension. 2019 Sep;74(3):555-563
Rats
Chronic constriction injury model
Intrathecal injection
100 μg/10 μL
Once daily for 5 days
L-NAME reversed the analgesic effect of HBO on neuropathic pain and decreased the expression of PKG1 mRNA and protein in the spinal dorsal horn
J Headache Pain. 2017 Dec;18(1):51
Spontaneously hypertensive rats
Spontaneously hypertensive rat model
Intraperitoneal injection
30 mg/kg
Single administration, lasting 6 hours
To investigate the effect of L-NAME on the blood pressure-lowering effect of the peptide AVFQHNCQE. The results showed that L-NAME completely abolished the antihypertensive effect of AVFQHNCQE, indicating that its antihypertensive effect is mediated by changes in endothelium-derived NO availability.
Nutrients. 2019 Jan 22;11(2):225
Wistar rats
L-NAME-induced hypertension model
Drinking water
40 mg/kg
Once daily for four weeks
To investigate the changes in cardiac function and the renin-angiotensin-aldosterone system in the L-NAME-induced hypertension model, and the protective effect of ivabradine. L-NAME increased systolic blood pressure and left ventricular weight, enhanced hydroxyproline concentration in the LV, and deteriorated LV function. Ivabradine reduced heart rate and systolic blood pressure, and improved LV function.
Inhibition of Nitric oxide synthase activity in mouse BV2 cells assessed as LPS-induced NO production after 24 hrs by Griess reaction, IC50=18.9 μM
21377368
mouse RAW264.7 cells
Function assay
17-20 h
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of IFN-gamma/LPS-stimulated nitric oxide production after 17 to 20 hrs by Griess assay, IC50=27.13 μM
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