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Journal articles on the topic 'Nitric oxide synthase'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Kim, Youngsun, Donghee Choi, Hosun Jang, Changsu Na, Moonhyeon Hwang, Joohyun Cho, Kyoungin Lee, Sunmin Kim, Byoungsik Pyo, and Daehwan Youn. "Effects of Acupuncture at ST41, BL60, GB38 on Changes of Nitric Oxide and Nitric Oxide Synthase in Rats." Korean Journal of Acupuncture 30, no. 2 (June 27, 2013): 97–103. http://dx.doi.org/10.14406/acu.2013.30.2.097.

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2

Ma, Li, and John L. Wallace. "Endothelial nitric oxide synthase modulates gastric ulcer healing in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 2 (August 1, 2000): G341—G346. http://dx.doi.org/10.1152/ajpgi.2000.279.2.g341.

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Nitric oxide has been shown to be beneficial for gastric ulcer healing. We determined the relative effects of endothelial and inducible nitric oxide synthases on gastric ulcer healing in rats. Ulcers were induced by serosal application of acetic acid. Ulcer severity, angiogenesis, and nitric oxide synthase expression were assessed 3–10 days later. The effects of inhibitors of nitric oxide synthase were also examined. Inducible nitric oxide synthase mRNA was only detected in ulcerated tissue (maximal at day 3), whereas the endothelial isoform mRNA was detected in normal tissue and increased during ulcer healing. Inducible nitric oxide synthase was expressed in inflammatory cells in the ulcer bed, whereas endothelial nitric oxide synthase was found in the vascular endothelium and in some mucosal cells in both normal and ulcerated tissues. Angiogenesis changed in parallel with endothelial nitric oxide synthase expression. N 6-(iminoethyl)-l-lysine did not affect angiogenesis or ulcer healing, while N G-nitro-l-arginine methyl ester significantly reduced both. In conclusion, endothelial nitric oxide synthase, but not the inducible isoform, plays a significant role in gastric ulcer healing.

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3

Yui, Yoshiki. "Nitric Oxide Synthase." Japanese Journal of Pharmacology 58 (1992): 17. http://dx.doi.org/10.1016/s0021-5198(19)37713-3.

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4

Han, Ji young, Younghwa Kim, Jeehye Sung, Yurry Um, Yi Lee, and Junsoo Lee. "Suppressive Effects of Chrysanthemum zawadskii var. latilobum Flower Extracts on Nitric Oxide Production and Inducible Nitric Oxide Synthase Expression." Journal of the Korean Society of Food Science and Nutrition 38, no. 12 (December 31, 2009): 1685–90. http://dx.doi.org/10.3746/jkfn.2009.38.12.1685.

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5

Kim, Ji-Soo, Hee-Jin Ahn, Hwa-Jeong Shin, Gyo-Jeong Gu, Sang-Hoon Eum, Chung-Ho Lee, In-Soon Min, and Hyung-Sun Youn. "Curcumin Inhibits Ovalbumin-Induced Inducible Nitric Oxide Synthase Expression." Korean Journal of Food Science and Technology 44, no. 4 (August 31, 2012): 498–501. http://dx.doi.org/10.9721/kjfst.2012.44.4.498.

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6

Lee, A.-Neum, Se-Jeong Park, Ae-Ri Jeong, Jae-Ran Lee, Hye-Jeong Park, Soo-Jung Kim, In-Soon Min, and Hyung-Sun Youn. "Ovalbumin Induces Cyclooxygenase-2 and Inducible Nitric Oxide Synthase Expression." Korean Journal of Food Science and Technology 43, no. 1 (February 28, 2011): 110–13. http://dx.doi.org/10.9721/kjfst.2011.43.1.110.

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7

Галкін, Б. М., В. О. Iваниця, and М. Б. Галкін. "BACTERIAL NITRIC OXIDE SYNTHASE." Microbiology&Biotechnology, no. 3(15) (September 15, 2011): 6–22. http://dx.doi.org/10.18524/2307-4663.2011.3(15).92878.

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8

Resink, Annelies, Valina L. Dawson, and Ted M. Dawson. "Nitric Oxide Synthase Inhibitors." CNS Drugs 6, no. 5 (November 1996): 351–57. http://dx.doi.org/10.2165/00023210-199606050-00002.

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9

Ghafourifar, Pedram. "Mitochondrial nitric oxide synthase." Frontiers in Bioscience 12, no. 1 (2007): 1072. http://dx.doi.org/10.2741/2127.

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10

Mulrennan, Siobhan A., and Anthony E. Redington. "Nitric Oxide Synthase Inhibition." Treatments in Respiratory Medicine 3, no. 2 (2004): 79–88. http://dx.doi.org/10.2165/00151829-200403020-00002.

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11

Smith, T. K., K. D. Wyatt, E. A. Buhr, K. J. Hildenbrand, and R. M. McAllister. "ENDOTHELIAL NITRIC OXIDE SYNTHASE." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S53. http://dx.doi.org/10.1097/00005768-200105001-00301.

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12

Frederiks, W. M. "Nitric oxide synthase activity." Journal of Histochemistry & Cytochemistry 44, no. 11 (November 1996): 1345–46. http://dx.doi.org/10.1177/44.11.8918910.

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13

DC, Widenka, Medele RJ, Stummer W, Bise K, and Steiger HJ. "Inducible nitric oxide synthase." Journal of Neurosurgical Anesthesiology 11, no. 4 (October 1999): 296. http://dx.doi.org/10.1097/00008506-199910000-00013.

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14

Rodríguez-Crespo, Ignacio, Nancy Counts Gerber, and Paul R. Ortiz de Montellano. "Endothelial Nitric-oxide Synthase." Journal of Biological Chemistry 271, no. 19 (May 10, 1996): 11462–67. http://dx.doi.org/10.1074/jbc.271.19.11462.

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15

Chen, Pei-Feng, Ah-Lim Tsai, Vladimir Berka, and Kenneth K. Wu. "Endothelial Nitric-oxide Synthase." Journal of Biological Chemistry 271, no. 24 (June 14, 1996): 14631–35. http://dx.doi.org/10.1074/jbc.271.24.14631.

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16

Soubrier, Florent. "Nitric Oxide Synthase Genes." Hypertension 33, no. 4 (April 1999): 924–26. http://dx.doi.org/10.1161/01.hyp.33.4.924.

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17

GHAFOURIFAR, P., and E. CADENAS. "Mitochondrial nitric oxide synthase." Trends in Pharmacological Sciences 26, no. 4 (April 2005): 190–95. http://dx.doi.org/10.1016/j.tips.2005.02.005.

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18

Brookes, Paul S. "Mitochondrial nitric oxide synthase." Mitochondrion 3, no. 4 (March 2004): 187–204. http://dx.doi.org/10.1016/j.mito.2003.10.001.

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19

Tai, Sharon C., G. Brett Robb, and Philip A. Marsden. "Endothelial Nitric Oxide Synthase." Arteriosclerosis, Thrombosis, and Vascular Biology 24, no. 3 (March 2004): 405–12. http://dx.doi.org/10.1161/01.atv.0000109171.50229.33.

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20

Rabelink, Ton J., and Thomas F. Luscher. "Endothelial Nitric Oxide Synthase." Arteriosclerosis, Thrombosis, and Vascular Biology 26, no. 2 (February 2006): 267–71. http://dx.doi.org/10.1161/01.atv.0000196554.85799.77.

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21

Gerber, Nancy Counts, and Paul R. Ortiz de Montellano. "Neuronal Nitric Oxide Synthase." Journal of Biological Chemistry 270, no. 30 (July 28, 1995): 17791–96. http://dx.doi.org/10.1074/jbc.270.30.17791.

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22

Oztuzcu, Serdar, Yusuf Ziya Igci, Ahmet Arslan, Ercan Sivasli, Esma Ozkara, Mehri Igci, Seniz Demiryürek, et al. "mRNA Expressions of Inducible Nitric Oxide Synthase, Endothelial Nitric Oxide Synthase, and Neuronal Nitric Oxide Synthase Genes in Meningitis Patients." Genetic Testing and Molecular Biomarkers 15, no. 3 (March 2011): 147–52. http://dx.doi.org/10.1089/gtmb.2010.0142.

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23

Rosbe, Kristina W., Jiri Prazma, Peter Petrusz, Whit Mims, Steve S. Ball, and Mark C. Weissler. "Third Place — Resident Basic Science Award 1995: Immunohistochemical Characterization of Nitric Oxide Synthase Activity in Squamous Cell Carcinoma of the Head and Neck." Otolaryngology–Head and Neck Surgery 113, no. 5 (November 1995): 541–49. http://dx.doi.org/10.1177/019459989511300504.

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This study was designed to investigate the presence of nitric oxide in human squamous cell carcinoma of the head and neck. We localized the activity of nitric oxide synthase in these tumors through immunohistochemical analysis using antibodies to L-citrulline (a byproduct of nitric oxide synthase), to inducible nitric oxide synthase, and to constitutive nitric oxide synthase. We found presence of inducible enzyme in squamous cells throughout these tumors, with the highest intensity staining occurring directly around keratin pearls. Our findings suggest that inducible nitric oxide synthase activity is present in squamous cell carcinomas of the head and neck, leading us to conclude that inducible nitric oxide synthase may play a significant role in tumor growth.

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24

Douglass, Matthew S., Yongmei Zhang, Mark R. Kaplowitz, and Candice D. Fike. "L-citrulline increases arginase II protein levels and arginase activity in hypoxic piglet pulmonary artery endothelial cells." Pulmonary Circulation 11, no. 2 (April 2021): 204589402110062. http://dx.doi.org/10.1177/20458940211006289.

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The L-arginine precursor, L-citrulline, re-couples endothelial nitric oxide synthase, increases nitric oxide production, and ameliorates chronic hypoxia-induced pulmonary hypertension in newborn pigs. L-arginine can induce arginase, which, in turn, may diminish nitric oxide production. Our major purpose was to determine if L-citrulline increases arginase activity in hypoxic piglet pulmonary arterial endothelial cells, and if so, concomitantly impacts the ability to increase endothelial nitric oxide synthase re-coupling and nitric oxide production. Piglet pulmonary arterial endothelial cells were cultured in hypoxic conditions with L-citrulline (0–3 mM) and/or the arginase inhibitor S-(2-boronoethyl)-L-cysteine. We measured arginase activity and nitric oxide production. We assessed endothelial nitric oxide synthase coupling by measuring endothelial nitric oxide synthase dimers and monomers. L-citrulline concentrations ≥0.5 mM increased arginase activity in hypoxic pulmonary arterial endothelial cells. L-citrulline concentrations ≥0.1 mM increased nitric oxide production and concentrations ≥0.5 mM elevated endothelial nitric oxide synthase dimer-to-monomer ratios. Co-treatment with L-citrulline and S-(2-boronoethyl)-L-cysteine elevated endothelial nitric oxide synthase dimer-to-monomer ratios more than sole treatment. Despite inducing arginase, L-citrulline increased nitric oxide production and endothelial nitric oxide synthase coupling in hypoxic piglet pulmonary arterial endothelial cells. However, these dose-dependent findings raise the possibility that there could be L-citrulline concentrations that elevate arginase to levels that negate improvements in endothelial nitric oxide synthase dysfunction. Moreover, our findings suggest that combining an arginase inhibitor with L-citrulline merits evaluation as a treatment for chronic hypoxia-induced pulmonary hypertension.

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25

Ravichandran, L. V., R. A. Johns, and A. Rengasamy. "Direct and reversible inhibition of endothelial nitric oxide synthase by nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 6 (June 1, 1995): H2216—H2223. http://dx.doi.org/10.1152/ajpheart.1995.268.6.h2216.

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The objective of this study was to investigate the regulation of endothelial nitric oxide (NO) synthase by NO. Partially purified endothelial NO synthase was exposed to authentic NO (10-200 microM) and to the nitrovasodilators sodium nitroprusside (SNP; 10-1,000 microM) and S-nitroso-N-acetylpenicillamine (SNAP; 100-1,000 microM), and enzyme activity was assayed by measuring the conversion of L-[3H]arginine to L-[3H]citrulline in the presence of added cofactors. NO, SNP, and SNAP inhibited NO synthase activity in a dose-dependent manner, NO being the most potent inhibitor. The Michaelis constant for L-arginine was not altered (4.87 microM) by NO (50 microM), whereas the maximal velocity of the enzyme decreased from 784 to 633 pmol.mg-1.min-1. Oxyhemoglobin (10 microM) partially prevented the inhibition of NO synthase by NO (50 microM). The data also suggest that NO inhibits endothelial NO synthase activity by directly interacting with the NO synthase and not by an indirect mechanism such as limitation of cofactor or oxygen availability. Dialysis of NO synthase treated with NO (50 microM) partially restored the enzyme activity. This study demonstrates a direct and reversible inhibition of NO synthase by NO, suggesting a feedback mechanism in vivo.

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26

Blute, Todd A., Bernd Mayer, and William D. Eldred. "Immunocytochemical and histochemical localization of nitric oxide synthase in the turtle retina." Visual Neuroscience 14, no. 4 (July 1997): 717–29. http://dx.doi.org/10.1017/s0952523800012670.

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AbstractRecent interest in nitric oxide and its relationship to cGMP has produced many attempts to anatomically localize the enzyme synthesizing nitric oxide, nitric oxide synthase. In the retina, numerous previous studies have used the NADPH-diaphorase enzyme activity of nitric oxide synthase as a histochemical method to localize nitric oxide synthase. However, all NADPH-diaphorase activity is not necessarily nitric oxide synthase, because several enzymes have similar biochemical activity. Additionally, various histochemical methods have been used to demonstrate NADPH-diaphorase activity, which makes comparisons between studies difficult. The purpose of this study was twofold. First, we wanted to examine the histochemical labeling of NADPH-diaphorase in the turtle retina to allow comparisons to previous studies. Second, we wanted to compare the histochemical localization of NADPH-diaphorase activity to the immunocytochemical localization of nitric oxide synthase in the turtle retina. Our histochemical localization of NADPH-diaphorase activity and our localization of nitric oxide synthase-like immunoreactivity in the turtle retina both produced similar results. Both the histochemistry and immunocytochemistry consistently labeled photoreceptor inner segments, at least three amacrine cell types, and processes in the inner plexiform layer. In optimized double-labeled preparations, all cells with NADPH-diaphorase activity were also positive for nitric oxide synthase-like immunoreactivity, although some somata in the ganglion cell layer only had nitric oxide synthase-like immunoreactivity. The immunocytochemical localization of nitric oxide synthase in photoreceptors, amacrine cells, and putative ganglion cells indicates that nitric oxide may function at several levels of visual processing in the turtle retina.

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27

Yavuz, Orhan, and Güngör Çağdaş Dinçel. "The Effect of Pneumonic Pasteurellosis on Apoptosis and Nitric Oxide Synthase in the Lungs in Calves." Turkish Journal of Agriculture - Food Science and Technology 8, no. 5 (May 30, 2020): 1166–70. http://dx.doi.org/10.24925/turjaf.v8i5.1166-1170.3337.

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Pneumonic Pasteurellosis (PP) is an infectious disease caused by Pasteurella multocida and Mannheimia haemolytica, mostly observed in cattle, sheep and calves. PP is characterized by fibrinous bronchopneumonia and pleuritis in the lungs. In this study, it was aimed to determine Caspase-3, Caspase-9, inducible nitric oxide synthase and neuronal nitric oxide synthase expressions by immunohistochemical methods in the lungs suffered from PP. For this purpose, twenty lung tissues were collected from calves with PP. For the Control Group, ten lungs of calves were collected from Aksaray Slaughterhouse. After necropsies of calves were confirmed to be PP by bacteriological examinations. Then the routine histological process was performed to tissues, and stained by Hematoxylin & Eosin for histopathology, and Caspase-3, Caspase-9, inducible nitric oxide synthase and neuronal nitric oxide synthase antibody staining for immunohistochemistry. The immunohistochemical findings indicated that Caspase-3, Caspase-9, inducible nitric oxide synthase and neuronal nitric oxide synthase positive reactions were seen in alveolar, bronchial and bronchiolar epithelia, and desquamated inflammatory cells in the lumens. In addition, the peripheral neural extensions were immunopositive for neuronal nitric oxide synthase and vascular endothelial cell were positive for inducible nitric oxide synthase. The findings can contribute to a better understanding of expressions of molecules such as Caspase and nitric oxide synthase. These results show that apoptosis and nitric oxide synthase expressions have triggered by airway epithelia and inflammatory cells in the lungs with Pneumonic Pasteurellosis in calves.

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28

del Rı́o, Luis A., F. Javier Corpas, and Juan B. Barroso. "Nitric oxide and nitric oxide synthase activity in plants." Phytochemistry 65, no. 7 (April 2004): 783–92. http://dx.doi.org/10.1016/j.phytochem.2004.02.001.

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29

Rothen, Hans Ulrich, and Daniel Schölly. "Nitric Oxide and Nitric Oxide Synthase Inhibitors in Sepsis." Digestive Surgery 13, no. 4-5 (1996): 425–29. http://dx.doi.org/10.1159/000172478.

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30

Busse, Rudi, and Ingrid Fleming. "Nitric oxide, nitric oxide synthase, and hypertensive vascular disease." Current Hypertension Reports 1, no. 1 (January 1999): 88–95. http://dx.doi.org/10.1007/s11906-999-0078-6.

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31

Deckel, A. Wallace. "Nitric oxide and nitric oxide synthase in Huntington's disease." Journal of Neuroscience Research 64, no. 2 (2001): 99–107. http://dx.doi.org/10.1002/jnr.1057.

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32

Zuo, Zhiyi, Alexandra Tichotsky, and Roger A. Johns. "Halothane and Isoflurane Inhibit Vasodilation Due to Constitutive but Not Inducible Nitric Oxide Synthase." Anesthesiology 84, no. 5 (May 1, 1996): 1156–65. http://dx.doi.org/10.1097/00000542-199605000-00018.

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Background Inhalational anesthetics inhibit the nitric oxide-guanylyl cyclase signaling pathway, but the site of this inhibition is not yet clear. This study was designed to test the hypothesis that receptor activation or downstream signaling events leading to nitric oxide synthase activation are important sites for this inhibition by comparing the effect of anesthetics on vasodilation caused by the calcium-dependent constitutive endothelial nitric oxide synthase versus the calcium-independent inducible nitric oxide synthase. Methods Endothelium-intact or -denuded rat thoracic aorta rings preincubated with or without lipopolysaccharide were mounted for isometric tension measurement, constricted with phenylephrine, then relaxed with methacholine in the presence or absence of halothane (1-3%) or isoflurane (1-3%). The cyclic guanosine 3,5-monophosphate content in the endothelium-denuded rings preincubated with or without lipopolysaccharide in the presence or absence of 3% halothane or 3% isoflurane was quantified by radioimmunoassay. The activity of partially purified inducible nitric oxide synthase from activated mouse macrophage was assayed in the presence or absence of halothane (1-4%) or isoflurane (1-5%) by the conversion of 3H-L-arginine to 3H-L-citrulline. Results Halothane and isoflurane inhibited methacholine-stimulated, nitric oxide-mediated vasorelaxation in endothelium-intact aortic rings. Neither halothane nor isoflurane affected the vasorelaxation caused by basal endothelial nitric oxide synthase or inducible nitric oxide synthase activity. Neither anesthetic altered the cyclic guanosine 3,5-monophosphate increase caused by inducible nitric oxide synthase in the lipopolysaccharide-treated rings. Conclusions The results demonstrated that halothane and isoflurane inhibit only receptor/calcium-activated nitric oxide synthase action and that direct inhibition of nitric oxide synthase, soluble guanylyl cyclase, or an interaction with nitric oxide are not responsible for anesthetic inhibition of endothelium-dependent vasorelaxation.

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33

Li, J., B. Shi, S. Yan, L. Jin, Y. Guo, and T. Li. "Effects of chitosan on nitric oxide production and inducible nitric oxide synthase activity and mRNA expression in weaned piglets." Czech Journal of Animal Science 60, No. 8 (April 9, 2018): 359–66. http://dx.doi.org/10.17221/8405-cjas.

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The effects of chitosan on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity and gene expression in vivo or vitro were investigated in weaned piglets. In vivo, 180 weaned piglets were assigned to five dietary treatments with six replicates. The piglets were fed on a basal diet supplemented with 0 (control), 100, 500, 1000, and 2000 mg chitosan/kg feed, respectively. In vitro, the peripheral blood mononuclear cells (PBMCs) from a weaned piglet were cultured respectively with 0 (control), 40, 80, 160, and 320 µg chitosan/ml medium. Results showed that serum NO concentrations on days 14 and 28 and iNOS activity on day 28 were quadratically improved with increasing chitosan dose (P < 0.05). The iNOS mRNA expressions were linearly or quadratically enhanced in the duodenum on day 28, and were improved quadratically in the jejunum on days 14 and 28 and in the ileum on day 28 (P < 0.01). In vitro, the NO concentrations, iNOS activity, and mRNA expression in unstimulated PBMCs were quadratically enhanced by chitosan, but the improvement of NO concentrations and iNOS activity by chitosan were markedly inhibited by N-(3-[aminomethyl] benzyl) acetamidine (1400w) (P < 0.05). Moreover, the increase of NO concentrations, iNOS activity, and mRNA expression in PBMCs induced by lipopolysaccharide (LPS) were suppressed significantly by chitosan (P < 0.05). The results indicated that the NO concentrations, iNOS activity, and mRNA expression in piglets were increased by feeding chitosan in a dose-dependent manner. In addition, chitosan improved the NO production in unstimulated PBMCs but inhibited its production in LPS-induced cells, which exerted bidirectional regulatory effects on the NO production via modulated iNOS activity and mRNA expression.

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34

Gokay, Nevzat Selim, Ibrahim Yilmaz, Baran Komur, Ahu Senem Demiroz, Alper Gokce, Sergülen Dervisoglu, and Banu Vural Gokay. "A Comparison of the Effects of Neuronal Nitric Oxide Synthase and Inducible Nitric Oxide Synthase Inhibition on Cartilage Damage." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/7857345.

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The objective of this study was to investigate the effects of selective inducible nitric oxide synthase and neuronal nitric oxide synthase inhibitors on cartilage regeneration. The study involved 27 Wistar rats that were divided into five groups. On Day 1, both knees of 3 rats were resected and placed in a formalin solution as a control group. The remaining 24 rats were separated into 4 groups, and their right knees were surgically damaged. Depending on the groups, the rats were injected with intra-articular normal saline solution, neuronal nitric oxide synthase inhibitor 7-nitroindazole (50 mg/kg), inducible nitric oxide synthase inhibitor amino-guanidine (30 mg/kg), or nitric oxide precursor L-arginine (200 mg/kg). After 21 days, the right and left knees of the rats were resected and placed in formalin solution. The samples were histopathologically examined by a blinded evaluator and scored on 8 parameters. Although selective neuronal nitric oxide synthase inhibition exhibited significant (P=0.044) positive effects on cartilage regeneration following cartilage damage, it was determined that inducible nitric oxide synthase inhibition had no statistically significant effect on cartilage regeneration. It was observed that the nitric oxide synthase activation triggered advanced arthrosis symptoms, such as osteophyte formation. The fact that selective neuronal nitric oxide synthase inhibitors were observed to have mitigating effects on the severity of the damage may, in the future, influence the development of new agents to be used in the treatment of cartilage disorders.

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35

Harper, Andrew, William R. Blythe, Carlton J. Zdanski, Jiri Prazma, and Harold C. Pillsbury. "Student Research Award 1994: Nitric Oxide in the Rat Vestibular System." Otolaryngology–Head and Neck Surgery 111, no. 4 (October 1994): 430–38. http://dx.doi.org/10.1177/019459989411100407.

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Nitric oxide is known to function as a neurotransmitter in the central nervous system. It is also known to be involved in the control nervous system excitatory amino acid neurotransmission cascade. Activation of excitatory amino acid receptors causes an influx of calcium, which activates nitric oxide synthase. The resulting increase in intracellular nitric oxide activates soluble guanylate cyclase, leading to a rise in cyclic guanosine monophosphate. The excitatory amino acids giutamate and aspartate are found in the vestibular system and have been postulated to function as vestibular system neurotransmitters. Although nitric oxide has ben investigated as a neurotransmitter in other tissues, no published studies have examined the role of nitric oxide in the vestibular system. Neuronal NADPH-dlaphorase has been characterized as a nitric oxide synthase. This enzyme catalyzes the conversion of L-arginine to l-citrulline, producing nitric oxide during the reaction. We used a histochemical stain characterized by Hope et al. (Proc Natl Acad Sci 1991;88:2811) as specific for neuronal nitric oxide synthase to localize the enzyme in the rat vestibular system. An Immunocytochemical stain was used to examine rat Inner ear tissue for the presence of the enzyme's end product, l-citrulline, thereby demonstrating nitric oxide synthase activity. Staining of vestibular ganglion sections showed nitric oxide synthase presence and activity in ganglion cells and nerve fibers. These results Indicate the presence of active nitric oxide synthase in these tissues and suggest modulation of vestibular neurotransmission by nitric oxide.

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36

Nevoral, J., T. Krejčová, J. Petr, P. Melicharová, A. Vyskočilová, M. Dvořáková, I. Weingartová, et al. "The role of nitric oxide synthase isoforms in aged porcine oocytes." Czech Journal of Animal Science 58, No. 10 (September 27, 2013): 453–59. http://dx.doi.org/10.17221/6994-cjas.

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In the sphere of reproductive biotechnologies, the demand for sufficient numbers of high-quality oocytes is still increasing. In some cases, this obstacle is overcome by in vitro prolonged cultivation. However, a prolonged oocyte culture is accompanied by changes called ageing. Ageing is manifested by spontaneous parthenogenetic activation, programmed cell death or lysis. Various substances, such as caffeine or dithiothreitol, have been tested for ageing suppression. In this respect, research into gasotransmitters (hydrogen sulphide, carbon monoxide, and nitric oxide) has currently been intensified. The objectives of the present study were to localize nitric oxide synthases (NOS) and to evaluate NOS inhibition of aged porcine oocytes. We demonstrated the presence of NOS isoforms in oocyte cultivation prolonged by 24, 48, and 72 h. After 72 h of prolonged cultivation, NOS inhibition by the non-specific inhibitor L-NAME or the specific inhibitor aminoguanidine caused suppression both of programmed cell death and lysis. Although NOS amount rapidly decreased after the 72-h cultivation, changes induced by NOS inhibition were statistically significant. We can presume that NOS play an important physiological role in porcine oocyte ageing.  

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37

Shin, Hwa-Jeong, and Hyung-Sun Youn. "Phenethyl Isothiocyanate Inhibits Ovalbumin-induced Inducible Nitric Oxide Synthase Expression." Korean Journal of Food Science and Technology 44, no. 6 (December 31, 2012): 759–62. http://dx.doi.org/10.9721/kjfst.2012.44.6.759.

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38

Rohrbach, Saskia, Arno Olthoff, Rainer Laskawi, and Werner Götz. "Neuronal Nitric Oxide Synthase-Immunoreactivity." ORL 64, no. 5 (2002): 330–34. http://dx.doi.org/10.1159/000066087.

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39

Miyazaki, Hiroshi, Hidehiro Matsuoka, John P. Cooke, Michiaki Usui, Seiji Ueda, Seiya Okuda, and Tsutomu Imaizumi. "Endogenous Nitric Oxide Synthase Inhibitor." Circulation 99, no. 9 (March 9, 1999): 1141–46. http://dx.doi.org/10.1161/01.cir.99.9.1141.

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40

Ghosh, Dipak K., Michael A. Holliday, Clayton Thomas, J. Brice Weinberg, Susan M. E. Smith, and John C. Salerno. "Nitric-oxide Synthase Output State." Journal of Biological Chemistry 281, no. 20 (February 3, 2006): 14173–83. http://dx.doi.org/10.1074/jbc.m509937200.

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41

Wood, Paul L., S. Choksi, and Virginia Bocchini. "Inducible microglial nitric oxide synthase." NeuroReport 5, no. 8 (April 1994): 977–80. http://dx.doi.org/10.1097/00001756-199404000-00031.

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Marletta, Michael A., Amy R. Hurshman, and Kristin M. Rusche. "Catalysis by nitric oxide synthase." Current Opinion in Chemical Biology 2, no. 5 (January 1998): 656–63. http://dx.doi.org/10.1016/s1367-5931(98)80098-7.

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Rauchhaus, M. "Nitric oxide synthase in CHF." European Heart Journal 21, no. 10 (May 15, 2000): 856–57. http://dx.doi.org/10.1053/euhj.1999.2004.

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Drouin, A., N. Thorin-Trescases, and E. Thorin. "Physiological endothelial nitric oxide synthase." Vascular Pharmacology 45, no. 3 (September 2006): e132-e133. http://dx.doi.org/10.1016/j.vph.2006.08.351.

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Boveris, Alberto, Laura B. Valdez, Silvia Alvarez, Tamara Zaobornyj, Alejandro D. Boveris, and Ana Navarro. "Kidney Mitochondrial Nitric Oxide Synthase." Antioxidants & Redox Signaling 5, no. 3 (June 2003): 265–71. http://dx.doi.org/10.1089/152308603322110841.

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Amin, Ashok R., Mukundan Attur, and Steven B. Abramson. "Nitric oxide synthase and cyclooxygenases." Current Opinion in Rheumatology 11, no. 3 (May 1999): 202–9. http://dx.doi.org/10.1097/00002281-199905000-00009.

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Leclercq, Baudouin, Edgar A. Jaimes, and Leopoldo Raij. "Nitric oxide synthase and hypertension." Current Opinion in Nephrology and Hypertension 11, no. 2 (March 2002): 185–89. http://dx.doi.org/10.1097/00041552-200203000-00009.

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Tejero, Jesús, and Dennis Stuehr. "Tetrahydrobiopterin in nitric oxide synthase." IUBMB Life 65, no. 4 (February 26, 2013): 358–65. http://dx.doi.org/10.1002/iub.1136.

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Förstermann, Ulrich, Ingolf Gath, Petra Schwarz, Ellen I. Closs, and Hartmut Kleinert. "Isoforms of nitric oxide synthase." Biochemical Pharmacology 50, no. 9 (October 1995): 1321–32. http://dx.doi.org/10.1016/0006-2952(95)00181-6.

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Pollock, Jennifer S., Ulrich Förstermann, W. Ross Tracey, and Masaki Nakane. "Nitric oxide synthase isozymes antibodies." Histochemical Journal 27, no. 10 (October 1995): 738–44. http://dx.doi.org/10.1007/bf02388299.

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