L nna

Manufactured by Merck Group

Sourced in United States, Germany, France

L-NNA is a laboratory reagent used in research applications. It is a nitric oxide synthase (NOS) inhibitor that can be used to study the role of nitric oxide in various biological processes. The core function of L-NNA is to inhibit the production of nitric oxide, which is a signaling molecule involved in various physiological and pathological processes.

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Lab products found in correlation

Indomethacin, by Merck Group (7 mentions) U46619, by Cayman Chemical (5 mentions) Mrs2500, by Bio-Techne (5 mentions) L name, by Merck Group (4 mentions) Phosphate buffered saline (pbs), by Thermo Fisher Scientific (4 mentions) Tempol, by Merck Group (3 mentions) Acetylcholine, by Merck Group (3 mentions) Ns 398, by Merck Group (3 mentions) Sc 560, by Merck Group (3 mentions) Tetrodotoxin, by Merck Group (3 mentions) Guanethidine, by Merck Group (2 mentions) Cay10441, by Cayman Chemical (2 mentions) U73122, by Cayman Chemical (2 mentions) Nf449, by Cayman Chemical (2 mentions) Alexa fluor 594, by Thermo Fisher Scientific (2 mentions) Vu0155069, by Santa Cruz Biotechnology (2 mentions) S mcpg, by Bio-Techne (2 mentions) Rhc 80267, by Enzo Life Sciences (2 mentions) Cay10594, by Santa Cruz Biotechnology (2 mentions) Nf023, by Merck Group (2 mentions)

Close spelling variants of this product

NG-nitro-L-arginine (L-NNA), Nω-nitro-L-arginine (L-NNA; N’-nitro-L-arginine (L-NNA) L-NG-Nitroarginine (L-NNA)

44 protocols using l nna

Investigating ACh Response with CAT Inhibitors

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To investigate the effect of CAT inhibitors on the acetylcholine response in human IMA, ring segments were divided into three groups and incubated with Krebs solution containing the NO synthase inhibitor, N^G-nitro-L-arginine (L-NNA, 100 µmol/L; Sigma-Aldrich) plus the cyclooxygenase inhibitor, indomethacin (10 µmol/L) (control); L-NNA plus indomethacin plus the CAT inhibitor, aminooxyacetic acid (AOAA, 100µmol/L; Sigma-Aldrich); or L-NNA plus indomethacin plus a competitive CAT substrate, L-aspartate (1000 µmol/L; Sigma-Aldrich). After equilibration for 45 min in the organ chamber, ring segments were pre-contracted with –8 log M of U-46619. Acetylcholine (−10 to −4.5 log M)-induced relaxation curves were then established.

Yuan C., Hou H.T., Chen H.X., Wang J., Wang Z.Q., Chen T.N., Novakovic A., Marinko M., Yang Q., Liu Z.G, & He G.W. (2019). Hydrogen sulfide-mediated endothelial function and the interaction with eNOS and PDE5A activity in human internal mammary arteries. The Journal of International Medical Research, 47(8), 3778-3791.

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Angiotensin-(1-7) Alleviates Stress-Induced Gastric Injury

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Rats were randomly divided into the following groups (8 rats each):
1) Control group (C); in which rats received no treatment and were left freely wandering in their cages for 3 hours after being subjected to pyloric ligation.
2) CRS group; in which rats received no treatment before exposure to CRS.
3) Stressed Ang-(1-7) treated group; in which rats were treated by Ang-(1-7) (6.5 mg/kg, i.p) (Sigma, USA) (11) one hour before exposure to CRS.
4) Stressed L-NNA-Ang-(1-7) treated group; in which the rats were treated by Ang-(1-7) (6.5 mg/kg, i.p.) thirty minutes after being treated by L-NNA (20 mg/kg, i.p) (Sigma, USA) (12) and after another thirty minutes rats were exposed to CRS.
5) Stressed Indo-Ang-(1-7) treated group; in which the rats were treated by Ang-(1-7) (6.5 mg/kg, i.p) thirty minutes after being treated by indomethacin (5 mg/kg /i.p) (Sigma, USA) (13) and after another thirty minutes rats were exposed to CRS.
Three hours after pyloric ligation, the rats were anesthetized by light ether anaesthesia, and blood samples were taken from the jugular vein. Then their stomachs were removed, opened along the greater curvature and the gastric content of each stomach was collected. The stomachs were washed with ice-cold saline and examined for gross gastric mucosal lesions using a magnifi ed lens by an observer not aware of the experiment.

A M.K., Aziz N.M., E M.A, & Rifaai R.A. (2016). Possible contribution of nitric oxide and prostaglandin in the protective effect of angiotensin (1-7) against stress induced gastric ulceration in adult male albino rats. Bratislavske lekarske listy, 117(12).

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Vasoactive Agents Pharmacology Study

Cited 1 time

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The drugs used in this study were: PA (PHL83553, Sigma, USA), indomethacin (PHR1247, Sigma, USA), L-phenylephrine chloride (PE) (PHR1017, Sigma, USA), acetylcholine chloride (A2662, Sigma, USA), L-NAME (N5752, Sigma, USA), L-NG-nitroarginine (L-NNA) (N5501, Sigma, USA), 1 H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (495,320, Sigma, USA). Indomethacin was dissolved in 0.1 M Na₂CO₃ solution. ODQ and PA were prepared in 20% dimethyl sulfoxide (DMSO). Others were dissolved in distilled water. The final concentration of DMSO in the bath was less than 0.5%, which had no influence on vasodilatation [12 (link)].

Li Z., Zhang F., Wang S., Xiao H., Wang J., Li X, & Yang H. (2022). Endothelium-dependent vasorelaxant effects of praeruptorin a in isolated rat thoracic aorta. Bioengineered, 13(4), 10038-10046.

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Perfusion Methodology for Tissue Imaging

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Tissues used for imaging and electrophysiological experiments were perfused with KRB solution containing (mM): NaCl, 120.35; KCl, 5.9; NaHCO₃, 15.5; NaH₂PO₄, 1.2; MgCl₂, 1.2; CaCl₂, 2.5; and glucose, 11.5. KRB solution was oxygenated with a mixture of 97% O₂/3% CO₂ and warmed to 37°C. For experiments using 0 mM [Ca²⁺]_o, CaCl₂ was excluded from the KRB solution and 0.5 mM EGTA was added, resulting in a Ca²⁺ free KRB solution. Ca²⁺ free Hanks’ solution contained the following (mM): NaCl, 125; KCl, 5.36; Glucose, 10; Sucrose, 2.9; NaHCO₃, 15.5; KH₂PO₄, 0.44; Na₂HPO₄, 0.33; Hepes, 10. The pH was adjusted to 7.4 with NaOH.
Nifedipine, nicardipine, atropine, guanethidine, L-NNA, CPA, tetracaine, caffeine, EGTA, and GSK 7975A were purchased from Sigma-Aldrich (St. Louis, MO, USA). Ani9 and MRS2500 was purchased from Tocris Bioscience (Ellisville, Missouri, USA). TTX was purchased from Abcam (Cambridge, MA, USA). Atropine, guanethidine, L-NNA, MRS2500, TTX, CPA, tetracaine and caffeine were diluted in deionized water. Nifedipine and nicardipine were diluted in ethanol. Ani9 was diluted in DMSO. All stock solutions of drugs were diluted to the desired final concentrations with KRB solution.

Drumm B.T., Hannigan K.I., Lee J.Y., Rembetski B.E., Baker S.A., Koh S.D., Cobine C.A, & Sanders K.M. (2022). Ca2+ signalling in interstitial cells of Cajal contributes to generation and maintenance of tone in mouse and monkey lower esophageal sphincters. The Journal of physiology, 600(11), 2613-2636.

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Comprehensive Pharmacological Reagents Catalog

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TTX, NBQX, D-AP5, S-MCPG, MRS2179 and A967079 were obtained from Tocris Biosciences; U46619, NF449, L-161982, U73122, CAY10441, PPOH, MAFP and FIPI from Cayman Chemicals; NS-398 and SC-560 from Calbiochem-Merck Millipore; RHC-80267 from Enzo Life Science; VU0155069 and CAY10594 from Santa Cruz; L-NNA, α,β-methylene ATP, NF023 and PGE₂ from Sigma; Alexa Fluor 488, Alexa Fluor 594, Fluo-4 pentapotassium salt, BAPTA tetrapotassium salt and Alexa Fluor 488 or FITC conjugated IB₄ from Life Technologies; and PBS and Alexa Fluor 633 hydrazide from Thermo Scientific. All other salts and reagents were purchased from Sigma.

Mishra A., Reynolds J.P., Chen Y., Gourine A.V., Rusakov D.A, & Attwell D. (2016). Astrocytes mediate neurovascular signaling to capillary pericytes but not to arterioles. Nature neuroscience, 19(12), 1619-1627.

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Pharmacological Tools for Vascular Function

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Mtx, ACh, tempol, L-NNA and indomethacin were purchased from Sigma-Aldrich (Tres Cantos, Madrid, Spain). SQ 29548 was obtained from Cayman Chemical Co. (Ann Harbor, MI).

Gonzalez-Paredes F.J., Hernández Mesa G., Morales Arraez D., Marcelino Reyes R., Abrante B., Diaz-Flores F., Salido E., Quintero E, & Hernández-Guerra M. (2016). Contribution of Cyclooxygenase End Products and Oxidative Stress to Intrahepatic Endothelial Dysfunction in Early Non-Alcoholic Fatty Liver Disease. PLoS ONE, 11(5), e0156650.

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Mesenteric Vascular Function Evaluation

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The mesenteric bed was immediately removed after animal sacrifice, and isolated mesenteric vessels with an average internal diameter of 250 μm were dissected and prepared as segments with intact PVAT and segments without PVAT. The vessels were studied using a multi-wire myograph system (Model 610 M, version 2.2; Danish Myo Technology) and analysed with ADInstruments Chart™ 5 (version 5.5.1). The vessels were bathed in physiologic saline solution (PSS; as above), maintained at 37°C and gassed with a mixture of 95% air and 5% CO₂. The vessels were normalised and their viability was checked by the addition of PSS containing 60 mM of KCl, following which concentration-response curves to norepinephrine (NE; A0937; Sigma-Aldrich) were constructed. To assess the effect of free radical scavengers on the obese PVAT, vessels from the obese cohort were incubated with superoxide dismutase (SOD; 100 U/ml; Sigma-Aldrich) and catalase (100 U/ml, Sigma-Aldrich) for 45 min, following which another NE concentration-response curve was constructed. Similarly, vessels were incubated with L-NNA (10^-4M, 45 min; Sigma-Aldrich) to assess NO bioavailability within PVAT. When required, removal of the endothelium was performed by a careful brushing technique using a 40-μm-diameter wire (the same as that used for myography) under visualisation by microscopy.

Aghamohammadzadeh R., Unwin R.D., Greenstein A.S, & Heagerty A.M. (2016). Effects of Obesity on Perivascular Adipose Tissue Vasorelaxant Function: Nitric Oxide, Inflammation and Elevated Systemic Blood Pressure. Journal of Vascular Research, 52(5), 299-305.

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Quantifying Nitric Oxide Levels in Vessels

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For DAF-FM staining, whole-mount cortical sections were incubated in Krebs-Hepes buffer with 20 μM freshly diluted DAF-FM diacetate (Invitrogen, D23844) for 60 min at room temperature. Samples were washed twice with PBS and washed in 0.1% Triton X-100 in PBS for 10 min before imaging. L-NNA (30 mg/kg in saline; Sigma-Aldrich) was administered intraperitoneally 48 and 24 hours before harvest and added during incubation at 1 mg/ml concentration. DAF-FM fluorescence intensity was quantified using ImageJ in three types of vessel segments grouped by their diameter: >60 (large), 35 to 55 (medium), and <30 μm (small). We left a 5-μm gap between the diameter bins to ensure clear separation between them. The L-NNA–sensitive intensity was calculated by subtracting values from L-NNA–treated samples for the same segment. Total nitrite and nitrate (NO₃ + NO₂) were measured using a commercially available fluorometric nitrite/nitrate assay kit according to the manufacturer’s instructions (Cayman Chemical). The assay is based on nitrite-mediated nitrosation of 2,3-diaminonaphthalene to a fluorescent triazole derivative under acidic conditions. Nitrate anion is reduced to nitrite with the help of nitrate reductase before nitrite measurements.

Huang L., Cheng F., Zhang X., Zielonka J., Nystoriak M.A., Xiang W., Raygor K., Wang S., Lakshmanan A., Jiang W., Yuan S., Hou K.S., Zhang J., Wang X., Syed A.U., Juric M., Takahashi T., Navedo M.F, & Wang R.A. (2023). Nitric oxide synthase and reduced arterial tone contribute to arteriovenous malformation. Science Advances, 9(21), eade7280.

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Isolated Vessel Experiments with aCSF

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Isolated vessel experiments were performed using aCSF (mM): NaCl 122.0, NaHCO₃ 26.0, KCl 3.0, NaH₂PO₄ 1.25, MgCl₂ 1.0, CaCl₂ 2.0, and glucose 4.0. Buffer solutions were made each week and stored without glucose at 4 °C. Glucose was added prior to each experiment. Zero calcium aCSF was made without the addition of CaCl₂. U46619, NS309, L-NNA, and SNP were purchased from Sigma (St. Louis, MO, USA). Stock solutions were made weekly and stored at 4° C for L-NNA and SNP. Aliquots of U46619 and NS309 were made and kept frozen at −20° C until use.

Chan S.L., Nelson M.T, & Cipolla M.J. (2018). Transient Receptor Potential Vanilloid-4 Channels Are Involved in Diminished Myogenic Tone in Brain Parenchymal Arterioles in Response to Chronic Hypoperfusion in Mice. Acta physiologica (Oxford, England), 225(2), e13181.

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Endothelial Cell Barrier Permeability Assay

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HRP‐conjugated anti‐mouse IgG, and rabbit IgG antibodies were purchased from Amersham Biosciences (Heidelberg, Germany); human thrombin from Behring (Marburg, Germany); anti VE‐cadherin (clone TEA 1, mouse IgG) from Beckman Coulter (Krefeld, Germany); ESI‐09 from Biolog (Bremen, Germany); benzonase, forskolin, myristoylated PKI, and Y‐27632, from Calbiochem (Darmstadt, Germany); anti‐phospho‐MLC and anti‐GAPDH antibodies from Cell signaling (Danvers, MA); Rac1 activation assay kit from cytoskeleton (Denver); Pierce^® ECL solution from Fischer Scientific (Niederlassung Nidderau, Germany); Alexa‐Flour labelled anti‐mouse IgG and anti‐rabbit IgG antibodies from Invitrogen (Karlsruhe, Germany); anti‐Rac1‐GTP antibody from NewEast Biosciences (King of Prussia, PA); EC basal medium plus supplement pack from PromoCell (Heidelberg, Germany); Complete^® protease inhibitor cocktail from Roche (Mannheim, Germany); 3‐isobutyl‐1‐methylxanthine (IBMX), Phalloidin‐TRITC, L‐NAME, L‐NNA, MDL‐12 330A, and anti‐vinculin (clone hVIN‐1, mouse IgG) from Sigma (Steinheim, Germany); anti‐phospho‐MYPT1 (Thr850) from Merck Millipore (Schwalbach, Germany), and Transwell polycarbonate membrane filters (24‐mm round) were from Greiner Bio‐One (Frickenhausen, Germany). All other chemicals were of the best available quality, usually analytical grade.

Aslam M., Tanislav C., Troidl C., Schulz R., Hamm C, & Gündüz D. (2014). cAMP controls the restoration of endothelial barrier function after thrombin‐induced hyperpermeability via Rac1 activation. Physiological Reports, 2(10), e12175.

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