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L-NAME hydrochloride Sale

(Synonyms: N'-硝基-L-精氨酸甲酯盐酸盐,L-NAME, L-NAME HCL) 目录号 : GA11233

L-NAME hydrochloride 抑制 NOS,IC50 为 70 μM。 L-NAME 是 NOS 抑制剂 L-NOARG 的前体,其 IC50 值为 1.4 μM。

L-NAME hydrochloride Chemical Structure

Cas No.:51298-62-5

规格 价格 库存 购买数量
1g
¥284.00
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5g
¥389.00
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10g
¥557.00
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25g
¥1,071.00
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Sample solution is provided at 25 µL, 10mM.

客户使用产品发表文献 1

实验参考方法

Cell experiment [1]:

Cell lines

Purified brain NOS

Preparation Method

L-NAME hydrochloride was added as 10 fold stock solutions of the respective hydrochlorides freshly prepared in water. For the bioactivation experiments aliquots of 10ul of the buffer,added to 90ul of the NOS reaction mixtures, yielding a theoretial final L-NAME concentration.

Reaction Conditions

0-1mM L-NAME hydrochloride for 24h

Applications

Freshly dissolved L-NAME was a inhibitor of purified brain NOS (mean IC50 = 70 μM), the apparent inhibitory potency of L-NAME approached that of L-NOARG upon prolonged incubation at neutral or alkaline pH.

Animal experiment [2]:

Animal models

Adult male Wistar rats (70–100 days of age) 

Preparation Method

Male Wistar rats were randomly assigned to control (C), L-NAME (L), chronic aerobic exercise (Ex), and chronic aerobic exercise associated to L-NAME (ExL). Aerobic training was performed with progressive intensity for 12 weeks; L-NAME was administered by orogastric gavage.

Dosage form

1.5 mg/kg/day L-NAME, oral gavage

Applications

Low-dose L-NAME alone did not change systolic blood pressure (SBP), but ExL significantly increased SBP at week 8 with normalization after 12 weeks. Furthermore, ExL promoted the elevation of left ventricle (LV) end-diastolic pressure without the presence of cardiac hypertrophy and fibrosis. Time to 50% shortening and relaxation were reduced in ExL, suggesting a cardiomyocyte contractile improvement. In conclusion, the association of chronic aerobic exercise and low-dose L-NAME prevented cardiac pathological remodeling and induced cardiomyocyte contractile function improvement

References:

[1]. Pfeiffer S, Leopold E, et al. Inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME): requirement for bioactivation to the free acid, NG-nitro-L-arginine. Br J Pharmacol. 1996 Jul;118(6):1433-40. 

[2]. Luchi TC, Coelho PM, et al. Lima-Leopoldo AP, Lunz W, Leopoldo AS. Chronic aerobic exercise associated to low-dose L-NAME improves contractility without changing calcium handling in rat cardiomyocytes. Braz J Med Biol Res. 2020 Mar 9;53(3):e8761.

产品描述

NG-nitro-L-arginine methyl ester (L-NAME) have been widely used to inhibit constitutive NO synthase (NOS) in different biological systems. L-NAME commonly used for the induction of NO-deficient hypertension?[1].

Freshly dissolved L-NAME was a 50 fold less potent inhibitor of purified brain NOS (mean IC50 = 70 μM) than L-NOARG (IC50 = 1.4 μM), but the apparent inhibitory potency of L-NAME approached that of L-NOARG upon prolonged incubation at neutral or alkaline pH. HPLC analyses revealed that NOS inhibition by L-NAME closely correlated with hydrolysis of the drug to L-NOARG[1].

IL-NAME and the related compound L-NA (100 μM) constricted pressurized vessels (Sprague–Dawley rats) with myogenic tone. Removal of the endothelium did not cause constriction or alter myogenic tone, however the constrictor effect of L-NAME persisted. The constrictor effect of L-NAME was abolished by L-arginine (1 mM)[2].

References:
[1]: Pfeiffer S, Leopold E, et al. Inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME): requirement for bioactivation to the free acid, NG-nitro-L-arginine. Br J Pharmacol. 1996 Jul;118(6):1433-40.
[2].Murphy TV, Kotecha N, et al. Endothelium-independent constriction of isolated, pressurized arterioles by Nomega-nitro-L-arginine methyl ester (L-NAME). Br J Pharmacol. 2007 Jul;151(5):602-9. doi: 10.1038/sj.bjp.0707262. Epub 2007 Apr 30.

NG-硝基-L-精氨酸甲酯 (L-NAME) 已广泛用于抑制不同生物系统中的组成型一氧化氮合酶 (NOS)。 L-NAME 通常用于诱导 NO 缺乏型高血压[1]

与 L-NOARG(IC50 = 1.4)相比,新鲜溶解的 L-NAME 对纯化脑 NOS 的抑制作用(平均 IC50 = 70 μM)低 50 倍μM),但在中性或碱性 pH 条件下长时间孵育后,L-NAME 的表观抑制效力接近 L-NOARG。 HPLC 分析表明,L-NAME 对 NOS 的抑制作用与药物水解为 L-NOARG 密切相关[1]

IL-NAME 和相关化合物 L-NA (100 μM) 收缩具有生肌张力的加压血管(Sprague-Dawley 大鼠)。去除内皮不会引起收缩或改变肌原性张力,但 L-NAME 的收缩效应仍然存在。 L-NAME 的收缩作用被 L-精氨酸 (1 mM)[2] 消除。

Chemical Properties

Cas No. 51298-62-5 SDF
别名 N'-硝基-L-精氨酸甲酯盐酸盐,L-NAME, L-NAME HCL
化学名 methyl (2S)-2-amino-5-[[amino(nitramido)methylidene]amino]pentanoate;hydrochloride
Canonical SMILES COC(=O)C(CCCN=C(N)N[N+](=O)[O-])N.Cl
分子式 C7H15N5O4.HCl 分子量 269.7
溶解度 ≥ 27mg/mL in Water, ≥ 23 mg/mL in DMSO 储存条件 Stored at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 3.7078 mL 18.5391 mL 37.0782 mL
5 mM 0.7416 mL 3.7078 mL 7.4156 mL
10 mM 0.3708 mL 1.8539 mL 3.7078 mL
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Research Update

Aortic Stiffness in L-NAME Treated C57Bl/6 Mice Displays a Shift From Early Endothelial Dysfunction to Late-Term Vascular Smooth Muscle Cell Dysfunction

Introduction and Aims: Endothelial dysfunction is recognized as a cardiovascular aging hallmark. Administration of nitric oxide synthase blocker N-Ω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) constitutes a well-known small animal model of cardiovascular aging. Despite extensive phenotypic characterization, the exact aortic function changes in L-NAME treated mice are largely unknown. Therefore, this study presents a longitudinal characterization of the aortic reactivity and biomechanical alterations in L-NAME treated C57Bl/6 mice. Methods and Results: Male C57Bl/6 mice were treated with L-NAME (0.5 mg/ml drinking water) for 1, 2, 4, 8, or 16 weeks. Peripheral blood pressure measurement (tail-cuff) and transthoracic echocardiograms were recorded, showing progressive hypertension after 4 weeks of treatment and progressive cardiac hypertrophy after 8-16 weeks of treatment. Aortic stiffness was measured in vivo as aortic pulse wave velocity (aPWV, ultrasound) and ex vivo as Peterson modulus (Ep). Aortic reactivity and biomechanics were investigated ex vivo in thoracic aortic rings, mounted isometrically or dynamically-stretched in organ bath set-ups. Aortic stiffening was heightened in L-NAME treated mice after all treatment durations, thereby preceding the development of hypertension and cardiac aging. L-NAME treatment doubled the rate of arterial stiffening compared to control mice, and displayed an attenuation of the elevated aortic stiffness at high distending pressure, possibly due to late-term reduction of medial collagen types I, III, and IV content. Remarkably, endothelial dysfunction, measured by acetylcholine concentration-response stimulation in precontracted aortic rings, was only observed after short-term (1-4 weeks) treatment, followed by restoration of endothelial function which coincided with increased phosphorylation of endothelial nitric oxide synthase (S1177). In the late-disease phase (8-16 weeks), vascular smooth muscle cell (VSMC) dysfunction developed, including increased contribution of voltage-dependent calcium channels (assessed by inhibition with diltiazem), basal VSMC cytoplasmic calcium loading (assessed by removal of extracellular calcium), and heightened intracellular contractile calcium handling (assessed by measurement of sarcoplasmic reticulum-mediated transient contractions). Conclusion: Arterial stiffness precedes peripheral hypertension and cardiac hypertrophy in chronic L-NAME treated male C57Bl/6 mice. The underlying aortic disease mechanisms underwent a distinct shift from early endothelial dysfunction to late-term VSMC dysfunction, with continued disease progression.

Hesperidin inhibits L-NAME-induced vascular and renal alterations in rats by suppressing the renin-angiotensin system, transforming growth factor-β1, and oxidative stress

The protective effect of hesperidin on vascular and renal alterations and possible underlying mechanisms involved in Nω -nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats were investigated in this study. Male Sprague-Dawley rats were administered L-NAME (40 mg/kg/day), L-NAME plus hesperidin (30 mg/kg/day), and L-NAME plus captopril (2.5 mg/kg/day) for 5 weeks. Hesperidin and captopril significantly prevented L-NAME-induced hypertension, vascular and renal dysfunction, intrarenal artery remodelling, glomerular extracellular matrix accumulation, and renal fibrosis. The preventive treatment with hesperidin and captopril also significantly decreased serum angiotensin-converting enzyme activity and plasma transforming growth factor-β1 (TGF-β1) levels and downregulated angiotensin II receptor type I and TGF-β1 protein expression in the kidneys. In addition, decreased malondialdehyde levels and increased superoxide dismutase activity in the plasma and kidney were observed after co-treatment with hesperidin or captopril. These findings suggest that hesperidin inhibits L-NAME-induced vascular and renal alterations in rats. The possible mechanism may be related to the suppression of the activation of the renin-angiotensin system and expression of TGF-β1, and reduction of oxidative stress.

Effect of 20-HETE inhibition on L-NAME-induced hypertension in rats

20-Hydroxyeicosatetraenoicacid (20-HETE) is an important mediator that regulates vascular tone and blood pressure (BP). Although various experimental animal hypertension models demonstrated that 20-HETE contributes to increased vascular resistance and BP, these effects have not been studied in Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension model. In this study, we investigated the effects of 20-HETE on the vascular responsiveness and BP in an L-NAME-induced hypertension. Wistar Albino rats were used in this study. Hypertension was induced by the addition of L-NAME to drinking water for 5 weeks. The study was performed in three stages: first, BP changes were monitored in real time in the presence of 20-HETE enzymatic inhibitor, N-hydroxy-N?-(4-butly-2-methylphenyl)-formamidine (HET-0016) for 1 h. Second, vascular responses of the conduit and resistance arteries were investigated in the presence or absence of HET-0016 in the organ bath. Third, BP was monitored weekly in some hypertensive animals treated with HET-0016 and vascular responses were investigated at the end of the experiment. We demonstrated an increase in 20-HETE levels in the resistance arteries of hypertensive animals. 20-HETE inhibition by HET-0016 significantly decreased BP in L-NAME-induced hypertension model. In addition, HET-0016 treatment caused significant improvement in vascular dilator and constrictor responses in the conduit and resistance arteries. This study demonstrates an important role of 20-HETE in increasing BP and altering vascular responsiveness in L-NAME-induced hypertension model, which suggests a possible involvement of 20-HETE in essential hypertension development in humans.

Clitoria ternatea L. extract prevents kidney damage by suppressing the Ang II/Nox4/oxidative stress cascade in l-NAME-induced hypertension model of rats

Clitoria ternatia L. (CT) has been reported to have anti-inflammatory and antioxidant effects. This study investigated the effect of CT aqueous flower extract on blood pressure and renal alterations in Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME)-induced hypertensive rats. Male Sprague Dawley rats received l-NAME in drinking water and were treated with CT flower extract or lisinopril. CT aqueous flower extract and lisinopril alleviated l-NAME-induced hypertension (p < 0.05). Glomerular extracellular matrix accumulation, renal fibrosis, and increased serum creatinine levels were observed in l-NAME-induced hypertensive rats and attenuated by CT flower extract or lisinopril co-treatment (p < 0.05). High levels of plasma angiotensin II (Ang II) and upregulated nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) protein expression in the kidneys induced by l-NAME were alleviated by CT flower extract or lisinopril co-treatment (p < 0.05). Furthermore, CT flower extract and lisinopril treatment reduced lipid peroxidation and elevated plasma and kidney malondialdehyde levels in l-NAME-induced hypertensive rats (p < 0.05). In conclusion, CT flower extract prevented l-NAME-induced renal injury and dysfunction in rats. The possible mechanism may be related to the suppression of Ang II-mediated Nox4 expression and the oxidative stress cascade in rats.

Effect of Lutein on L-NAME-Induced Hypertensive Rats

We investigated the antihypertensive effect of lutein on N(G) -nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Daily oral administration of L-NAME (40 mg/kg)-induced a rapid progressive increase in mean arterial pressure (MAP). L-NAME significantly increased MAP from the first week compared to that in the control and reached 193.3±9.6 mmHg at the end of treatment. MAP in the lutein groups was dose-dependently lower than that in the L-NAME group. Similar results were observed for systolic and diastolic blood pressure of L-NAME-induced hypertensive rats. The control group showed little change in heart rate for 3 weeks, whereas L-NAME significantly reduced heart rate from 434±26 to 376±33 beats/min. Lutein (2 mg/kg) significantly prevented the reduced heart rate induced by L-NAME. L-NAME caused hypertrophy of heart and kidney, and increased plasma lipid peroxidation four-fold but significantly reduced plasma nitrite and glutathione concentrations, which were significantly prevented by lutein in a dose-dependent manner. These findings suggest that lutein affords significant antihypertensive and antioxidant effects against L-NAME-induced hypertension in rats.