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Journal articles on the topic 'Nitroindazole'

Author: Grafiati

Published: 24 April 2022

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1

Eddahmi, Mohammed, Nuno M. M. Moura, Latifa Bouissane, Ouafa Amiri, M. Amparo F. Faustino, José A. S. Cavaleiro, Ricardo F. Mendes, Filipe A. A. Paz, Maria G. P. M. S. Neves, and El Mostapha Rakib. "A Suitable Functionalization of Nitroindazoles with Triazolyl and Pyrazolyl Moieties via Cycloaddition Reactions." Molecules 25, no. 1 (December 28, 2019): 126. http://dx.doi.org/10.3390/molecules25010126.

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The alkylation of a series of nitroindazole derivatives with 1,2-dibromoethane afforded the corresponding N-(2-bromoethyl)- and N-vinyl-nitro-1H-indazoles. The Cu(I)-catalysed azide- alkyne 1,3-dipolar cycloaddition was selected to substitute the nitroindazole core with 1,4-disubstituted triazole units after converting one of the N-(2-bromoethyl)nitroindazoles into the corresponding azide. The reactivity in 1,3-dipolar cycloaddition reactions with nitrile imines generated in situ from ethyl hydrazono-α-bromoglyoxylates was studied with nitroindazoles bearing a vinyl unit. The corresponding nitroindazole-pyrazoline derivatives were obtained in good to excellent yields.

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2

Ooms, Frédéric, Bernadette Norberg, Emre M. Isin, Neal Castagnoli, Cornelis J. Van der Schyf, and Johan Wouters. "7-Nitroindazole." Acta Crystallographica Section C Crystal Structure Communications 56, no. 10 (October 15, 2000): e474-e475. http://dx.doi.org/10.1107/s0108270100011975.

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3

IBÁÑEZ-ESCRIBANO, ALEXANDRA, JUAN JOSÉ NOGAL-RUIZ, ALICIA GÓMEZ-BARRIO, VICENTE J. ARÁN, and JOSÉ ANTONIO ESCARIO. "In vitro trichomonacidal activity and preliminary in silico chemometric studies of 5-nitroindazolin-3-one and 3-alkoxy-5-nitroindazole derivatives." Parasitology 143, no. 1 (November 4, 2015): 34–40. http://dx.doi.org/10.1017/s0031182015001419.

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SUMMARYA selection of 1,2-disubstituted 5-nitroindazolin-3-ones (1–19) and 3-alkoxy-5-nitroindazoles substituted at positions 1 (20–24) or 2 (25–39) from our in-house compound library were screened in vitro against the most common curable sexually transmitted pathogen, Trichomonas vaginalis. A total of 41% of the studied molecules (16/39) achieved a significant activity of more than 85% growth inhibition at the highest concentration assayed (100 µg mL−1). Among these compounds, 3-alkoxy-5-nitroindazole derivatives 23, 24, 25 and 27 inhibited parasite growth by more than 50% at 10 µg mL−1. In addition, the first two compounds (23, 24) still showed remarkable activity at the lowest dose tested (1 µg mL−1), inhibiting parasite growth by nearly 40%. Their specific activity towards the parasite was corroborated by the determination of their non-specific cytotoxicity against mammalian cells. The four mentioned compounds exhibited non-cytotoxic profiles at all of the concentrations assayed, showing a fair antiparasitic selectivity index (SI > 7·5). In silico studies were performed to predict pharmacokinetic properties, toxicity and drug-score using Molinspiration and OSIRIS computational tools. The current in vitro results supported by the virtual screening suggest 2-substituted and, especially, 1-substituted 3-alkoxy-5-nitroindazoles as promising starting scaffolds for further development of novel chemical compounds with the main aim of promoting highly selective trichomonacidal lead-like drugs with adequate pharmacokinetic and toxicological profiles.

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Saunders, Fiona D., Martin Westphal, Perenlei Enkhbaatar, Jianpu Wang, Konrad Pazdrak, Yoshimitsu Nakano, Atsumori Hamahata, et al. "Molecular biological effects of selective neuronal nitric oxide synthase inhibition in ovine lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 3 (March 2010): L427—L436. http://dx.doi.org/10.1152/ajplung.00147.2009.

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Neuronal nitric oxide synthase is critically involved in the pathogenesis of acute lung injury resulting from combined burn and smoke inhalation injury. We hypothesized that 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, blocks central molecular mechanisms involved in the pathophysiology of this double-hit insult. Twenty-five adult ewes were surgically prepared and randomly allocated to 1) an uninjured, untreated sham group ( n = 7), 2) an injured control group with no treatment ( n = 7), 3) an injury group treated with 7-nitroindazole from 1-h postinjury to the remainder of the 24-h study period ( n = 7), or 4) a sham-operated group subjected only to 7-nitroindazole to judge the effects in health. The combination injury was associated with twofold increased activity of neuronal nitric oxide synthase and oxidative/nitrosative stress, as indicated by significant increases in plasma nitrate/nitrite concentrations, 3-nitrotyrosine (an indicator of peroxynitrite formation), and malondialdehyde lung tissue content. The presence of systemic inflammation was evidenced by twofold, sixfold, and threefold increases in poly(ADP-ribose) polymerase, IL-8, and myeloperoxidase lung tissue concentrations, respectively (each P < 0.05 vs. sham). These molecular changes were linked to tissue damage, airway obstruction, and pulmonary shunting with deteriorated gas exchange. 7-Nitroindazole blocked, or at least attenuated, all these pathological changes. Our findings suggest 1) that nitric oxide formation derived from increased neuronal nitric oxide synthase activity represents a pivotal reactive agent in the patho-physiology of combined burn and smoke inhalation injury and 2) that selective neuronal nitric oxide synthase inhibition represents a goal-directed approach to attenuate the degree of injury.

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Gutiérrez-Sánchez, Gaizka, Ignacio García-Alonso, Jorge Gutiérrez Sáenz de Santa María, Ana Alonso-Varona, and Borja Herrero de la Parte. "Antioxidant-Based Therapy Reduces Early-Stage Intestinal Ischemia-Reperfusion Injury in Rats." Antioxidants 10, no. 6 (May 27, 2021): 853. http://dx.doi.org/10.3390/antiox10060853.

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Intestinal ischemia-reperfusion injury (i-IRI) is a rare disorder with a high mortality rate, resulting from the loss of blood flow to an intestinal segment. Most of the damage is triggered by the restoration of flow and the arrival of cytokines and reactive oxygen species (ROS), among others. Inactivation of these molecules before tissue reperfusion could reduce intestinal damage. The aim of this work was to analyze the preventive effect of allopurinol and nitroindazole on intestinal mucosal damage after i-IRI. Wag/RijHsd rats were subjected to i-IRI by clamping the superior mesenteric artery (for 1 or 2 h) followed by a 30 min period of reperfusion. Histopathological intestinal damage (HID) was assessed by microscopic examination of histological sections obtained from injured intestine. HID was increased by almost 20% by doubling the ischemia time (from 1 to 2 h). Nitroindazole reduced HID in both the 1 and 2 h period of ischemia by approximately 30% and 60%, respectively (p < 0.001). Our preliminary results demonstrate that nitroindazole has a preventive/protective effect against tissue damage in the early stages of i-IRI. However, to better understand the molecular mechanisms underlying this phenomenon, further studies are needed.

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Editorial, E. "Retraction: 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor in vivo prevents kainate-induced intrahippocampal neurotoxicity. Radenovic L, Selakovic V, Bozic B. Arch Biol Sci. 2005;57(2)75-81. DOI: 10.2298/ABS0502075R." Archives of Biological Sciences 68, no. 3 (2016): 691. http://dx.doi.org/10.2298/abs160412036e.

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The article: 7-Nitroindazole, a selective neuronal nitric oxide synthase inhibitor in vivo prevents kainate-induced intrahippocampal neurotoxicity. Radenovic L, Selakovic V, Bozic B. Arch Biol Sci. 2005;57(2)75-81, repeats data already published in: 7-Nitroindazole reduces nitrite concentration in rat brain after intrahippocampal kainate-induced seizure. Radenovic L, Vasiljevic I, Selakovic V, Jovanovic M. Comp Biochem Physiol Pt. C. 2003;135 443-50, without any referencing. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS0502075R">10.2298/ABS0502075R</a></b></u>

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7

Wiciński, M., G. Grześk, B. Malinowski, E. Grześk, A. T. Sinjab, M. Krzyżanowski, A. Michalska, et al. "Imidazole-induced contractility of vascular smooth muscle cells in the presence of U-73122, ODQ, indomethacin and 7-nitroindazole." Polish Journal of Veterinary Sciences 16, no. 2 (June 1, 2013): 293–97. http://dx.doi.org/10.2478/pjvs-2013-0040.

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Abstract The aim of the study was to assess the impact of modulating factors on vascular smooth muscle cells reactivity. Vascular resistance was induced by the administration of increasing concentrations of imidazole. The experiments were performed on isolated and perfused tail artery of Wistar rats (weight 250 g - 350 g). Rats were been narcotized by urethane (intraperitoneal injection) at a dose of 120 mg/kg, stunned and then sacrificed by cervical dislocation. In the following investigation classical pharmacometric methods were used. Relationships between concentration-response curves (CRCs) for imidazole observed in the presence of ODQ [(1H-(1,2,4)oxadiazolo-[4,3-a]quinoxalin-1-one)], 7-nitroindazole and indomethacin were analyzed. Imidazole-induced contractility of vascular smooth muscle cells was independent from alpha- adrenergic receptors and PLC activity. Reactivity of VSMCsinduced by imidazole, was significantly changed in the presence of ODQ and 7-nitroindazole.

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Radenovic, Lidija, Vesna Selakovic, and Biljana Bozic. "7-nitroindazole, a selective neuronal nitric oxide synthase inhibitore in vivo, prevents kainate-induced intrahippocampal neurotoxicity." Archives of Biological Sciences 57, no. 2 (2005): 75–81. http://dx.doi.org/10.2298/abs0502075r.

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We investigated the effects of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. 7-nitroindazole can effectively inhibit NO synthesis in rat brain after kainate-induced neurotoxicity and suppressed nitrite accumulation. The present results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href="http://dx.doi.org/10.2298/ABS160412036E">10.2298/ABS160412036E</a><u></b></font>

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9

Jellestad, Finn Konow, and Hilde Gundersen. "Behavioral effects of 7-nitroindazole on hyperbaric oxygen toxicity." Physiology & Behavior 76, no. 4-5 (August 2002): 611–16. http://dx.doi.org/10.1016/s0031-9384(02)00765-5.

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10

Aerschot, A. Van, J. Rozenski, D. Loakes, N. Pillet, G. Schepers, and P. Herdewijn. "An acyclic 5-nitroindazole nucleoside analogue as ambiguous nucleoside." Nucleic Acids Research 23, no. 21 (1995): 4363–70. http://dx.doi.org/10.1093/nar/23.21.4363.

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11

Arán, Vicente J., Carmen Ochoa, Lucı́a Boiani, Pablo Buccino, Hugo Cerecetto, Alejandra Gerpe, Mercedes González, et al. "Synthesis and biological properties of new 5-nitroindazole derivatives." Bioorganic & Medicinal Chemistry 13, no. 9 (May 2005): 3197–207. http://dx.doi.org/10.1016/j.bmc.2005.02.043.

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12

Nováková, Kateřina, Vojtěch Hrdlička, Tomáš Navrátil, Vlastimil Vyskočil, and Jiří Barek. "Determination of 5-nitroindazole using silver solid amalgam electrode." Monatshefte für Chemie - Chemical Monthly 146, no. 5 (December 10, 2014): 761–69. http://dx.doi.org/10.1007/s00706-014-1346-y.

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13

Bostanci, M. Ömer, and Faruk Bağirici. "Neuroprotection by 7-Nitroindazole Against Iron-Induced Hippocampal Neurotoxicity." Cellular and Molecular Neurobiology 27, no. 7 (October 27, 2007): 933–41. http://dx.doi.org/10.1007/s10571-007-9223-4.

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14

Eddahmi, Mohammed, Vera Sousa, Nuno M. M. Moura, Cristina J. Dias, Latifa Bouissane, Maria A. F. Faustino, José A. S. Cavaleiro, et al. "New nitroindazole-porphyrin conjugates: Synthesis, characterization and antibacterial properties." Bioorganic Chemistry 101 (August 2020): 103994. http://dx.doi.org/10.1016/j.bioorg.2020.103994.

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15

Kuz'menko, V. V., and A. F. Pozharskii. "Synthesis and some properties of 1-amino-3-nitroindazole." Chemistry of Heterocyclic Compounds 32, no. 10 (October 1996): 1152–55. http://dx.doi.org/10.1007/bf01169225.

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Farias, Martin, Keith Jackson, Michael Johnson, and James L. Caffrey. "Cardiac enkephalins attenuate vagal bradycardia: interactions with NOS-1-cGMP systems in canine sinoatrial node." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (November 2003): H2001—H2012. http://dx.doi.org/10.1152/ajpheart.00275.2003.

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Endogenous opioids and nitric oxide (NO) are recognized modulators of cardiac function. Enkephalins and inhibitors of NO synthase (NOS) both produce similar interruptions in the vagal control of heart rate. This study was conducted to test the hypothesis that NO systems within the canine sinoatrial (SA) node facilitate local vagal transmission and that the endogenous enkephalin methionine-enkephalin-arginine-phenylalanine (MEAP) attenuates vagal bradycardia by interrupting the NOS-cGMP pathway. Microdialysis probes were inserted into the SA node, and they were perfused with nonselective ( Nω-nitro-l-arginine methyl ester) and neuronal (7-nitroindazole) NOS inhibitors. The right vagus nerve was stimulated and both inhibitors gradually attenuated the resulting vagal bradycardia. The specificity of these inhibitions was verified by an equally gradual reversal of the inhibition with an excess of the NOS substrate l-arginine. Introduction of MEAP into the nodal interstitium produced a quickly developing but quantitatively similar interruption of vagal bradycardia that was also slowly reversed by the addition of l-arginine and not by d-arginine. Additional support for convergence of opioid and NO pathways was provided when the vagolytic effects of MEAP were also reversed by the addition of the NO donor S-nitroso- N-acetyl-penicillamine, the protein kinase G activator 8-bromo-cGMP, or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. MEAP and 7-nitroindazole were individually combined with the direct acting muscarinic agonist methacholine to evaluate potential interactions with muscarinic receptors within the SA node. MEAP and 7-nitroindazole were unable to overcome the bradycardia produced by methacholine. These data suggest that NO and enkephalins moderate the vagal control of heart rate via interaction with converging systems that involve the regulation of cAMP within nodal parasympathetic nerve terminals.

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Liu, Xiaoguang, Chunyuan Li, John R. Falck, Richard J. Roman, David R. Harder, and Raymond C. Koehler. "Interaction of nitric oxide, 20-HETE, and EETs during functional hyperemia in whisker barrel cortex." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 2 (August 2008): H619—H631. http://dx.doi.org/10.1152/ajpheart.01211.2007.

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Nitric oxide (NO) modulates vasodilation in cerebral cortex during sensory activation. NO is known to inhibit the synthesis of 20-HETE, which has been implicated in arteriolar constriction during astrocyte activation in brain slices. We tested the hypothesis that the attenuated cerebral blood flow (CBF) response to whisker stimulation seen after NO synthase (NOS) inhibition requires 20-HETE synthesis and that the ability of an epoxyeicosatrienoic acids (EETs) antagonist to reduce the CBF response is blunted after NOS inhibition but restored with simultaneous blockade of 20-HETE synthesis. In anesthetized rats, the increase in CBF during whisker stimulation was attenuated after the blockade of neuronal NOS with 7-nitroindazole. Subsequent administration of the 20-HETE synthesis inhibitor N-hydroxy- N′-(4-n-butyl-2-methylphenyl)formamidine (HET0016) restored the CBF response to control levels. After the administration of 7-nitroindazole, the inhibitory effect of an EETs antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) on the CBF response was lost, whereas the simultaneous administration of 7-nitroindazole and HET0016 restored the inhibitory effect of 14,15-EEZE. The administration of HET0016 alone had only a small effect on the evoked CBF response in rats. Furthermore, in neuronal NOS+/+ and NOS−/− mice, HET0016 administration did not increase the CBF response to whisker stimulation. In neuronal NOS+/+ mice, HET0016 also blocked the reduction in the response seen with acute NOS inhibition. These results indicate that 20-HETE synthesis normally does not substantially restrict functional hyperemia. Increased NO production during functional activation may act dynamically to suppress 20-HETE synthesis or downstream signaling and permit EETs-dependent vasodilation. With the chronic loss of neuronal NOS in mice, other mechanisms apparently suppress 20-HETE synthesis or signaling.

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Gautier, Henry, and Cristina Murariu. "Role of nitric oxide in hypoxic hypometabolism in rats." Journal of Applied Physiology 87, no. 1 (July 1, 1999): 104–10. http://dx.doi.org/10.1152/jappl.1999.87.1.104.

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Because it has been recently suggested that nitric oxide (NO) may mediate the effects of hypoxia on body temperature and ventilation, the present study was designed to assess more completely the effects of a neuronal NO synthase inhibitor (7-nitroindazole, 25 mg/kg ip), at ambient temperature of 26 and 15°C, on the ventilatory (V˙), metabolic (O2 consumption), and thermal changes (colonic and tail temperatures) induced by ambient hypoxia (fractional inspired O2 of 11%) or CO hypoxia (fractional inspired CO of 0.07%) in intact, unanesthetized adult rats. At both ambient temperatures, 7-nitroindazole decreased oxygen consumption, colonic temperature, andV˙ in normoxia. The drug reduced ambient or CO hypoxia-induced hypometabolism and ventilatory response, but the hypothermia persisted. It is concluded that NO arising from neural NO synthase plays an important role in the control of metabolism andV˙ in normoxia. As well, it mediates, in part, the hypometabolic and the ventilatory response to hypoxia. The results are consistent with the notion that central nervous system hypoxia resets the thermoregulatory set point by decreasing brain NO.

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Maksimovic, Ivana, Marina Jovanovic, Miodrag Colic, Dejan Micic, Rosa Mihajlovic, and Vesna Selakovic. "Nitric oxide synthase inhibitors prevents quinolinic acid-induced neurotoxicity: the role of nitric oxide and glucose-6-phosphate dehydrogenase in cell death." Jugoslovenska medicinska biohemija 21, no. 3 (2002): 269–74. http://dx.doi.org/10.2298/jmh0203269m.

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In the present study we employed Nw-nitro-L-arginine methyl ester, non-specific potent nitric oxide synthase inhibitor and a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, reportedly to investigate the possible involvement of nitric oxide in quinolinic acid-induced striatal toxicity in the rat. Quinolinic acid was administered unilaterally into striatum of adult Wistar rats in the single dose of 150 nmol/L. The other two group of animals were pretreated with Nw-nitro-L-arginine methyl ester and 7-nitroindazole respectively. Control groups of animals were treated with 0,154 mmol/L saline solution likewise. Nitrite levels was decreased in the ipsi- and contralateral striatum and forebrain cortex in the group treated with nitric oxide synthase inhibitors and neurotoxin compared to quinolinic acid-treated animals. In the same structures, activity of glucose-6-phosphate dehydrogenase was also decreased, compared to quinolinic acid-treated animals. These results indicate that application of the nitric oxide synthase inhibitors, supressed nitrite accumulation and glucose-6-phosphate dehydrogenase activity and attenuated quinolinic acid-induced neuronal damage in the striatum and forebrain cortex.

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Alexander, J., R. Pruitt, M. Lyon, A. B. Whitehead, and C. N. Karson. "115. Potential neuroleptic properties of central NOS-inhibitor 7-nitroindazole." Biological Psychiatry 43, no. 8 (April 1998): S35. http://dx.doi.org/10.1016/s0006-3223(98)90563-7.

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SAMADHIYA, PUSHKAL, RITU SHARMA, SANTOSH K. SRIVASTAV, and SAVITRI D. SRIVASTAVA. "SYNTHESIS OF 4-THIAZOLIDINE DERIVATIVES OF 6-NITROINDAZOLE: PHARMACEUTICAL IMPORTANCE." Journal of the Chilean Chemical Society 57, no. 1 (March 2012): 1036–43. http://dx.doi.org/10.4067/s0717-97072012000100018.

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Prchal, Vit, Anita Ottenschlagerova, Vlastimil Vyskocil, and Jiri Barek. "Voltammetric Determination of 5-nitroindazole using a Bismuth Bulk Electrode." Analytical Letters 49, no. 1 (April 11, 2015): 49–55. http://dx.doi.org/10.1080/00032719.2014.996810.

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Wangensteen, Rosemary, Isabel Rodríguez-Gómez, Juan Manuel Moreno, Miriam Álvarez-Guerra, Antonio Osuna, and Félix Vargas. "Effects of chronic treatment with 7-nitroindazole in hyperthyroid rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (November 2006): R1376—R1382. http://dx.doi.org/10.1152/ajpregu.00722.2005.

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This study analyzed the contribution of neuronal nitric oxide synthase (nNOS) to the hemodynamic manifestations of hyperthyroidism. The effects on hyperthyroid rats of the chronic administration of 7-nitroindazole (7-NI), an inhibitor of nNOS, were studied. Six groups of male Wistar rats were used: control, 7-NI (30 mg·kg−1·day−1 by gavage), T450, T475 (50 or 75 μg thyroxine·rat−1·day−1, respectively), T450+7-NI, and T475+7-NI. All treatments were maintained for 4 wk. Body weight, tail systolic blood pressure (SBP), and heart rate (HR) were recorded weekly. Finally, SBP, pulse pressure (PP), and HR were measured in conscious rats, and morphological, metabolic, plasma, and renal variables were determined. Expression of nNOS in the hypothalamus of T475 and control rats was analyzed by Western blot analysis. The response of mean arterial pressure (MAP) to pentolinium (10 mg/kg iv) was used to evaluate the sympathetic contribution to BP in T475 and T475+7-NI rats. T4 produced an increased hypothalamic nNOS expression and dose-related increases in blood pressure (BP), HR, and PP vs. control rats. 7-NI did not modify BP or any other hemodynamic variable in normal rats. However, 7-NI produced a marked reduction in BP, HR, PP, and food and water intake in both hyperthyroid groups and improved creatinine clearance in the T475 group. Pentolinium produced a greater MAP decrease in the T475+7-NI than in the T475 group. In conclusion, administration of 7-NI attenuates the hemodynamic and metabolic manifestations of hyperthyroidism, suggesting that nNOS contributes to the hyperdynamic circulation of this endocrine disease by modulating sympathetic activity.

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Ribeiro da Silva, Manuel A. V., and Joana I. T. A. Cabral. "Standard molar enthalpies of formation of 5- and 6-nitroindazole." Journal of Thermal Analysis and Calorimetry 100, no. 2 (January 27, 2010): 457–64. http://dx.doi.org/10.1007/s10973-009-0648-5.

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Fabricius, M., I. Rubin, M. Bundgaard, and M. Lauritzen. "NOS activity in brain and endothelium: relation to hypercapnic rise of cerebral blood flow in rats." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (November 1, 1996): H2035—H2044. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h2035.

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We examined whether attenuation of the hypercapnic increase of cerebral blood flow (CBF) associated with nitric oxide synthase (NOS) inhibition is related to local neuronal or aortic endothelial NOS activity or local endothelial/neuronal NOS-dependent vasodilation. Halothane-anesthetized rats were ventilated, and CBF was measured by laser-Doppler flowmetry over the parietal and cerebellar cortex. Intravenous N omega-nitro-L-arginine (L-NNA; 30 mg/kg) inhibited brain and aortic NOS activity by 67-70%. Topical L-NNA (1 mM) inhibited brain NOS activity by 91-94%, whereas aortic NOS activity remained constant. In contrast, intravenous L-NNA attenuated the hypercapnic CBF rise much more efficiently than topical L-NNA. 7-Nitroindazole, another NOS inhibitor, attenuated endothelial and neuronal NOS activity equally well and inhibited the hypercapnic CBF increase as effectively as L-NNA. Topical L-NNA and 7-nitroindazole abolished local endothelial NOS-dependent vasodilation after 15 min, whereas hypercapnic CBF was only slightly reduced. L-NNA injected into the tissue abolished neuronal NOS-dependent vasodilation, whereas hypercapnic CBF was unchanged. The findings suggest that local NOS activity, whether neuronal or endothelial, is unimportant for the hypercapnic rise of CBF.

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Tyurenkov, I. N., T. A. Popova, V. N. Perfilova, I. I. Prokofiev, A. V. Borisov, M. V. Kustova, G. I. Zaypullaev, and O. V. Ostrovskij. "Protective effects of a new glutamic acid derivative against stress after nNOS blockade." Biomeditsinskaya Khimiya 63, no. 1 (January 2017): 47–55. http://dx.doi.org/10.18097/pbmc20176301047.

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We studied the effects of a new glutamic acid derivative, glufimet, on oxidative stress, activity of antioxidant enzymes, mitochondrial respiration, endothelial vasodilation and anti-platelet activity in female rats after exposure to 24-hour immobilization pain stress and 7-nitroindazole, a neuronal nitric oxide synthase (nNOS) inhibitor. A single dose administration of glufimet (29 mg/kg intraperitoneally) 10 minutes before stress exposure caused a decrease of NO metabolites in serum (by 27.2%) and heart homogenate (33.5% (p£0.05), respectively, compared with the control group. Administration of 7-nitroindazole with glufimet also decreased the studied parameters by 14.3% in the heart homogenate and by 30,3% in the brain (p£0.05) compared with stress exposed rats receiving only the nNOS inhibitor. Glufimet decreased the levels of primary and secondary products of lipid peroxidation (LPO), conjugated dienes by 20% (p£0.05) and 17.3% (p£0.05), ketodienes by 16% and 13.7%, malondialdehyde by 15% (p£0.05) and 26.6% (p£0.05) in the heart and brain mitochondria of stress exposed rats, respectively, compared with the control group. Glufimet administration also increased SOD activity (by 14.4% and 13.1%, respectively), catalase (by 19% and 26.8%, respectively) and glutathione peroxidase (GPx) activity (by 45.5% (p£0.05) and 7.3%, respectively). The antioxidant effect of glufimet may be also attributed to increased coupling between the processes of mitochondria respiration and oxidative phosphorylation. This was evidenced by an increase in the respiratory control ratio (RCR) (by 46.0% (p£0.05) for malate/glutamate and by 49,7% (p£0.05) for succinate) in the heart mitochondria. A statistically significant increase in RCR (by 37.3% (p£0.05)) was observed in stress exposed female rat brain mitochondria for succinate. RCRs differed significantly for succinate in the heart and brain of rats receiving glufimet after nNOS blockade. RCR increased by 62.3% (p£0.05) in the heart mitochondria and by 72.2% (p£0.05) in the brain mitochondria compared with the RCRs in stress exposed rats receiving 7-nitroindazole.

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Hardy, P., D. Lamireau, X. Hou, I. Dumont, D. Abran, A. M. Nuyt, D. R. Varma, and S. Chemtob. "Major role for neuronal NO synthase in curtailing choroidal blood flow autoregulation in newborn pig." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1655–62. http://dx.doi.org/10.1152/jappl.2001.91.4.1655.

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We examined whether nitric oxide (NO) generated from neuronal NO synthase (nNOS) contributes to the reduced ability of the newborn to autoregulate retinal blood flow (RBF) and choroidal blood flow (ChBF) during acute rises in perfusion pressure. In newborn pigs (1–2 days old), RBF (measured by microsphere) is autoregulated over a narrow range of perfusion pressure, whereas ChBF is not autoregulated. N G-nitro-l-arginine methyl ester (l-NAME) or specific nNOS inhibitors 7-nitroindazole, 3-bromo-7-nitroindazole, and 1-(2-trifluoromethyl-phenyl)imidazole as well as ganglionic blocker hexamethonium, unveiled a ChBF autoregulation as observed in juvenile (4- to 6-wk old) animals, whereas autoregulation of RBF in the newborn was only enhanced byl-NAME. All NOS inhibitors and hexamethonium prevented the hypertension-induced increase in NO mediator cGMP in the choroid. nNOS mRNA expression and activity were three- to fourfold higher in the choroid of newborn pigs than in tissues of juvenile pigs. It is concluded that increased production of NO from nNOS curtails ChBF autoregulation in the newborn and suggests a role for the autonomic nervous system in this important hemodynamic function, whereas, for RBF autoregulation, endothelial NOS seems to exert a more important contribution in limiting autoregulation.

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Vasiljevic, Ivana, Marina Jovanovic, Miodrag Colic, Rosa Mihajlovic, Mirjana Djukic, Milica Ninkovic, and Zivorad Malicevic. "Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats." Jugoslovenska medicinska biohemija 23, no. 1 (2004): 11–18. http://dx.doi.org/10.2298/jmh0401011v.

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The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease.

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Bitterman, Noemi, and Haim Bitterman. "l-Arginine-NO pathway and CNS oxygen toxicity." Journal of Applied Physiology 84, no. 5 (May 1, 1998): 1633–38. http://dx.doi.org/10.1152/jappl.1998.84.5.1633.

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The involvement of thel-arginine-nitric oxide (NO) pathway in the pathogenesis of hyperoxia-induced seizures was studied by using agents controlling NO levels. We selected two inhibitors of nitric oxide synthase, the systemic inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) and the novel cerebral-specific inhibitor 7-nitroindazole, and two generators of NO, the NO donor S-nitroso- N-acetylpenicillamine and the physiological precursorl-arginine. Rats with chronic cortical electrodes were injected intraperitoneally with different doses of one of the agents or their vehicles before exposure to 0.5 MPa O2 and O2 with 5% CO2 at an absolute pressure of 0.5 MPa. The duration of the latent period until the onset of electrical discharges in the electroencephalogram was used as an index of central nervous system O2 toxicity. The two nitric oxide synthase inhibitorsl-NAME and 7-nitroindazole significantly prolonged the latent period to the onset of seizures on exposure to both hyperbaric O2 and to the hypercapnic-hyperoxic mixture. Pretreatment with the NO donor S-nitroso- N-acetylpenicillamine significantly shortened the latent period, whereasl-arginine, the physiological precursor of NO, significantly prolonged the latent period to onset of seizures. Our results suggest that thel-arginine-NO pathway is involved in the pathophysiology of hyperoxia-induced seizures via various regulating mechanisms.

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30

Wazlawik, Elisabeth, and Gina S. Morato. "Effects of intracerebroventricular administration of 7-nitroindazole on tolerance to ethanol." Brain Research Bulletin 57, no. 2 (January 2002): 165–70. http://dx.doi.org/10.1016/s0361-9230(01)00736-5.

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31

Olea-Azar, Claudio, Hugo Cerecetto, Alejandra Gerpe, Mercedes González, Vicente J. Arán, Carolina Rigol, and Lucía Opazo. "ESR and electrochemical study of 5-nitroindazole derivatives with antiprotozoal activity." Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy 63, no. 1 (January 2006): 36–42. http://dx.doi.org/10.1016/j.saa.2005.04.011.

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32

KUZ'MENKO, V. V., and A. F. POZHARSKII. "ChemInform Abstract: Synthesis and Some Properties of 1-Amino-3-nitroindazole." ChemInform 28, no. 13 (August 4, 2010): no. http://dx.doi.org/10.1002/chin.199713090.

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USAREWICZ, J., U. WRZECIONO, Z. LUKASZEWSKI, B. GATNIEJEWSKA, and K. PEISERT. "ChemInform Abstract: Azoles. Part 32. Nitroindazole Derivatives and Their Electron Affinity." ChemInform 23, no. 36 (August 21, 2010): no. http://dx.doi.org/10.1002/chin.199236155.

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Gzella, Andrzej, and Urszula Wrzeciono. "Azole. 47. Über 3-Thiomorpholino- und 3-(4-Methylpiperazino)-5-nitroindazole." Acta Crystallographica Section C Crystal Structure Communications 57, no. 10 (October 12, 2001): 1189–91. http://dx.doi.org/10.1107/s0108270101011027.

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35

Anaeigoudari, Akbar, Mohammad Naser Shafei, Mohammad Soukhtanloo, Hamid Reza Sadeghnia, Parham Reisi, Farimah Beheshti, Reza Mohebbati, Seyed Mojtaba Mousavi, and Mahmoud Hosseini. "Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole." Arquivos de Neuro-Psiquiatria 73, no. 9 (September 2015): 784–90. http://dx.doi.org/10.1590/0004-282x20150121.

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Inflammation and oxidative stress have important roles in memory impairment. The effect of 7-nitroindazole (7NI) on lipopolysaccharide (LPS)-induced memory impairment was investigated. Rats were used, divided into four groups that were treated as follows: (1) control (saline); (2) LPS; (3) 7NI-LPS; and (4) 7NI before passive avoidance (PA). In the LPS group, the latency for entering the dark compartment was shorter than in the controls (p < 0.01 and p < 0.001); while in the 7NI-LPS group, it was longer than in the LPS group (p < 0.01 and p < 0.001). Malondialdehyde (MDA) and nitric oxide (NO) metabolite concentrations in the brain tissues of the LPS group were higher than in the controls (p < 0.001 and p < 0.05); while in the 7NI-LPS group, they were lower than in the LPS group (p < 0.001 and p < 0.05, respectively). The thiol content in the brain of the LPS group was lower than in the controls (p < 0.001); while in the 7NI-LPS group, it was higher than in the LPS group (p < 0.001). It is suggested that brain tissue oxidative damage and NO elevation have a role in the deleterious effects of LPS on memory retention that are preventable using 7NI.

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Cheptea, C., L. M. Ivan, D. O. Dorohoi, V. Sunel, I. Hurjui, C. I. Saveanu, and A. I. Galaction. "Optimized Synthesis and Spectral Characterization of Some Hydrazones Based on 5-Nitroindazole with Pharmacological Potential." Ukrainian Journal of Physics 59, no. 3 (March 2014): 313–18. http://dx.doi.org/10.15407/ujpe59.03.0313.

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37

Huang, An, Dong Sun, Edward G. Shesely, Ellen M. Levee, Akos Koller, and Gabor Kaley. "Neuronal NOS-dependent dilation to flow in coronary arteries of male eNOS-KO mice." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 2 (February 1, 2002): H429—H436. http://dx.doi.org/10.1152/ajpheart.00501.2001.

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Flow-induced dilation was examined in isolated coronary arteries of endothelial nitric oxide (NO) synthase knockout mice (eNOS-KO) and wild-type (WT) mice. The basal tone of arteries (percentage of passive diameter) was significantly greater in eNOS-KO than in WT mice; their flow-induced dilations, however, were similar. Endothelial removal eliminated the dilations in vessels of both strains of mice. In arteries of WT mice, N ω-nitro-l-arginine methyl ester (l-NAME) (10−4 M) or indomethacin (10−5 M) alone, inhibited flow-induced dilation by ∼50%, whereas their simultaneous administration abolished the responses. In arteries of eNOS-KO mice, flow-induced dilation was inhibited by ∼40% with l-NAME. The residual portion (60%) of the response was eliminated by the additional administration of indomethacin. 7-Nitroindazole (10−4 M) attenuated flow-induced dilation by ∼40% in arteries of eNOS-KO mice, but did not affect responses in those of WT mice. 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (3 × 10−5 M) inhibited thel-NAME/7-nitroindazole-sensitive portion of the responses in arteries of eNOS-KO mice. Immunohistochemical evidence confirms the presence of neuronal NOS (nNOS) in the arterial endothelium of eNOS-KO mice. In conclusion, nNOS-derived NO, via activation of cGMP, together with prostaglandins, maintains flow-induced dilation in coronary arteries of male eNOS-KO mice.

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38

Yildiz, F., G. Ulak, B. F. Erden, and N. Gacar. "Anxiolytic-Like Effects of 7-Nitroindazole in the Rat Plus-Maze Test." Pharmacology Biochemistry and Behavior 65, no. 2 (February 2000): 199–202. http://dx.doi.org/10.1016/s0091-3057(99)00133-1.

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39

Borowicz, Kinga K., Zdzisław Kleinrok, and Stanisław J. Czuczwar. "Influence of 7-nitroindazole on the anticonvulsive action of conventional antiepileptic drugs." European Journal of Pharmacology 331, no. 2-3 (July 1997): 127–32. http://dx.doi.org/10.1016/s0014-2999(97)01034-0.

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40

Kelly, Paul A. T., Isobel M. Ritchie, and Douglas E. McBean. "7-Nitroindazole reduces cerebral blood flow following chronic nitric oxide synthase inhibition." Brain Research 885, no. 2 (December 2000): 295–97. http://dx.doi.org/10.1016/s0006-8993(00)02980-2.

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41

Manzanedo, Carmen, Marı́a A. Aguilar, Marta Rodrı́guez-Arias, Miguel Navarro, and José Miñarro. "7-Nitroindazole blocks conditioned place preference but not hyperactivity induced by morphine." Behavioural Brain Research 150, no. 1-2 (April 2004): 73–82. http://dx.doi.org/10.1016/s0166-4328(03)00225-0.

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42

Escott, K. J., J. S. Beech, B. S. Meldrum, S. C. R. Williams, and P. M. W. Bath. "Delayed treatment of reversible focal cerebral ischaemia with 7-nitroindazole in rats." Journal of Hypertension 14, no. 12 (December 1996): 1511–12. http://dx.doi.org/10.1097/00004872-199612000-00042.

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43

Zagvazdin, Yuri, Anton Reiner, and Ibrahim F. Benter. "How Selective Is 7-Nitroindazole, An Inhibitor of Neuronal Nitric Oxide Synthase?" Anesthesia & Analgesia 86, no. 3 (March 1998): 679. http://dx.doi.org/10.1097/00000539-199803000-00056.

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44

Kahn, Ronald A., Jesse Weinberger, and Michael Panah. "How Selective Is 7-Nitroindazole, An Inhibitor of Neuronal Nitric Oxide Synthase?" Anesthesia & Analgesia 86, no. 3 (March 1998): 679–80. http://dx.doi.org/10.1097/00000539-199803000-00057.

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45

Zagvazdin, Yuri, Anton Reiner, and Ibrahim F. Benter. "How Selective Is 7-Nitroindazole, An Inhibitor of Neuronal Nitric Oxide Synthase?" Anesthesia & Analgesia 86, no. 3 (March 1998): 679. http://dx.doi.org/10.1213/00000539-199803000-00056.

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46

Kahn, Ronald A., Jesse Weinberger, and Michael Panah. "How Selective Is 7-Nitroindazole, An Inhibitor of Neuronal Nitric Oxide Synthase?" Anesthesia & Analgesia 86, no. 3 (March 1998): 679–80. http://dx.doi.org/10.1213/00000539-199803000-00057.

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47

Tabuchi, Keiji, Kazuhiko Takahashi, Zenya Ito, Akira Hara, Tetsuro Wada, and Jun Kusakari. "Effect of 7-Nitroindazole upon Cochlear Dysfunction Induced by Transient Local Anoxia." Annals of Otology, Rhinology & Laryngology 109, no. 8 (August 2000): 715–19. http://dx.doi.org/10.1177/000348940010900803.

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48

Fonseca-Berzal, Cristina, Alexandra Ibáñez-Escribano, Nerea Vela, José Cumella, Juan José Nogal-Ruiz, José Antonio Escario, Patrícia Bernardino da Silva, et al. "Antichagasic, Leishmanicidal, and Trichomonacidal Activity of 2-Benzyl-5-nitroindazole-Derived Amines." ChemMedChem 13, no. 12 (May 22, 2018): 1246–59. http://dx.doi.org/10.1002/cmdc.201800084.

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49

Callahan, Brian T., and George A. Ricaurte. "Effect of 7-nitroindazole on body temperature and methamphetamine-induced dopamine toxicity." NeuroReport 9, no. 12 (August 1998): 2691–95. http://dx.doi.org/10.1097/00001756-199808240-00001.

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50

Iadecola, C., G. Yang, and S. Xu. "7-Nitroindazole attenuates vasodilation from cerebellar parallel fiber stimulation but not acetylcholine." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 4 (April 1, 1996): R914—R919. http://dx.doi.org/10.1152/ajpregu.1996.270.4.r914.

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We used the relatively selective inhibitor of neuronal nitric oxide synthase 7-nitroindazole (7-NI) to test the hypothesis that the increases in local cerebellar blood flow (BFcrb) elicited by activation of the cerebellar parallel fibers (PF) are mediated by neuronal production of nitric oxide. In halothane-anesthetized rats, the cerebellar cortex was exposed and superfused with Ringer solution (37 degrees C; pH 7.3-7.4). The PF were stimulated electrically (100 microA, 30 Hz, 40 s), while BFcrb was monitored at the site of stimulation by a laser-Doppler flow probe. In vehicle-treated rats (n = 5), PF stimulation increased BFcrb by 61 +/- 5% (P < 0.05; analysis of variance and Tukey's test). 7-NI attenuated the increase in BFcrb dose dependently (10-100 mg/kg i.p.; n = 5 animals/dose) and by 55 +/- 7% at 100 mg/kg (P < 0.05). The attenuation of the response to PF stimulation was correlated with the degree of inhibition of calcium-dependent brain nitric oxide synthase activity, measured ex vivo by the citrulline assay (n = 21). 7-NI also attenuated the cerebrovasodilation elicited by hypercapnia (PCO2 = 50-60 mmHg) but did not affect the vasodilation evoked by acetylcholine (10 microM; n = 4; P > 0.05; t-test), a response mediated by endothelial nitric oxide synthase. 7-NI did not attenuate the BFcrb increase evoked by the nitric oxide donor S-nitroso-N-acetylpenicillamine (1 mM; n = 5; P > 0.05; t-test). Similarly, 7-NI did not affect resting systemic arterial pressure. These observations suggest that selective inhibition of neuronal nitric oxide synthase by 7-NI attenuates the increases in BFcrb evoked by PF stimulation. The findings provide additional support to the hypothesis that the increase in BFcrb evoked by PF stimulation is mediated, in part, by glutamate-induced activation of neuronal nitric oxide synthase.

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