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Journal articles on the topic 'Neuronal nitric oxide synthase (nNOS)'

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Published: 4 June 2021

Last updated: 4 February 2022

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1

Kourosh-Arami, Masoumeh, Nasrin Hosseini, Monireh Mohsenzadegan, Alireza Komaki, and Mohammad Taghi Joghataei. "Neurophysiologic implications of neuronal nitric oxide synthase." Reviews in the Neurosciences 31, no. 6 (August 27, 2020): 617–36. http://dx.doi.org/10.1515/revneuro-2019-0111.

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AbstractThe molecular and chemical properties of neuronal nitric oxide synthase (nNOS) have made it a key mediator in many physiological functions and signaling transduction. The NOS monomer is inactive, but the dimer form is active. There are three forms of NOS, which are neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) nitric oxide synthase. nNOS regulates nitric oxide (NO) synthesis which is the mechanism used mostly by neurons to produce NO. nNOS expression and activation is regulated by some important signaling proteins, such as cyclic adenosine monophosphate (cAMP) response elem

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2

Huber, Andrea, Dieter Saur, Manfred Kurjak, Volker Schusdziarra, and Hans-Dieter Allescher. "Characterization and splice variants of neuronal nitric oxide synthase in rat small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 5 (November 1, 1998): G1146—G1156. http://dx.doi.org/10.1152/ajpgi.1998.275.5.g1146.

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The aim of this study was to characterize neuronal nitric oxide synthase (nNOS) activity and 5′-end splice variants in rat small intestine. nNOS was predominantly expressed in the longitudinal muscle layer, with attached myenteric plexus (LM-MP). The biochemical properties of NOS activity in enriched nerve terminals resemble those of nNOS isolated from the brain. Western blot analysis of purified NOS protein with an nNOS antibody showed a single band in the particulate fraction and three bands in the soluble fraction. Rapid amplification of 5′ cDNA ends-PCR revealed the presence of three diffe

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3

Rao, Y. Manjula, Arun Chaudhury, and Raj K. Goyal. "Active and inactive pools of nNOS in the nerve terminals in mouse gut: implications for nitrergic neurotransmission." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 3 (March 2008): G627—G634. http://dx.doi.org/10.1152/ajpgi.00519.2007.

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Nitric oxide (NO) is responsible for nitrergic neurotransmission in the gut, and its release is dependent on its de novo synthesis by neuronal nitric oxide synthase (nNOS). The magnitude of NO synthesis and release during neurotransmission may be related to the fraction of catalytically active nNOS out of a larger pool of inactive nNOS in the nerve terminals. The purpose of the present study was to identify catalytically active and inactive pools of nNOS in the varicosities from mouse gut. Enteric varicosities were confirmed as nitrergic by colocalization of nNOS with the nerve varicosity mark

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4

Di Giacomo, C., V. Sorrenti, L. Salerno, V. Cardile, F. Guerrera, M. A. Siracusa, M. Avitabile, and A. Vanella. "Novel Inhibitors of Neuronal Nitric Oxide Synthase." Experimental Biology and Medicine 228, no. 5 (May 2003): 486–90. http://dx.doi.org/10.1177/15353702-0322805-11.

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Selective inhibitors of neuronal nitric oxide synthase (nNOS), which are devoid of any effect on the endothelial isoform (eNOS), may be required for the treatment of some neurological disorders. In our search for novel nNOS inhibitors, we recently described some 1-[(Aryloxy)ethyl]-1 H-imidazoles as interesting molecules for their selectivity for nNOS against eNOS. This work reports a new series of 1-[(Aryloxy)alkyl]-1 H-imidazoles in which a longer methylene chain is present between the imidazole and the phenol part of molecule. Some of these molecules were found to be more potent nNOS inhibit

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5

YONEYAMA, Hirohito, Akira YAMAMOTO, and Hiroaki KOSAKA. "Neuronal nitric oxide synthase generates superoxide from the oxygenase domain." Biochemical Journal 360, no. 1 (November 8, 2001): 247–53. http://dx.doi.org/10.1042/bj3600247.

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When l-arginine is depleted, neuronal nitric oxide synthase (nNOS) has been reported to generate superoxide. A flavoprotein module construct of nNOS has been demonstrated to be sufficient for superoxide production. In contrast, nNOS was reported not to be involved in superoxide formation, because such formation occurred with a mixture of the boiled enzyme and redox-active cofactors. We aimed to resolve these controversial issues by examining superoxide generation, without the addition of redox-active cofactors, by recombinant wild-type nNOS and by C415A-nNOS, which has a mutation in the haem p

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6

González-Martínez, Jorge A., Gabriel Möddel, Zhong Ying, Richard A. Prayson, William E. Bingaman, and Imad M. Najm. "Neuronal nitric oxide synthase expression in resected epileptic dysplastic neocortex." Journal of Neurosurgery 110, no. 2 (February 2009): 343–49. http://dx.doi.org/10.3171/2008.6.17608.

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Object Nitric oxide has been associated with epileptogenesis. Previous studies have shown increased expression of N-methyl-d-aspartate (NMDA) subunit NR2B receptors in epileptic dysplastic human neocortex. The expression of neuronal nitric oxide synthase (nNOS), and its relation to this subunit NR2B in epileptic dysplastic tissue has never been addressed. Methods Ten patients with medically intractable epilepsy caused by focal cortical dysplasia (CD), and 2 patients with mesial temporal sclerosis (control group) underwent pre- and/or intraoperative invasive monitoring evaluations. Cortical sam

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7

Premaratne, Shyamal, Chun Xue, John M. McCarty, Muhammad Zaki, Robert W. McCuen, Roger A. Johns, Wolfgang Schepp, et al. "Neuronal nitric oxide synthase: expression in rat parietal cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 2 (February 1, 2001): G308—G313. http://dx.doi.org/10.1152/ajpgi.2001.280.2.g308.

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Nitric oxide synthases (NOS) are enzymes that catalyze the generation of nitric oxide (NO) from l-arginine and require nicotinamide adenine dinucleotide phosphate (NADPH) as a cofactor. At least three isoforms of NOS have been identified: neuronal NOS (nNOS or NOS I), inducible NOS (iNOS or NOS II), and endothelial NOS (eNOS or NOS II). Recent studies implicate NO in the regulation of gastric acid secretion. The aim of the present study was to localize the cellular distribution and characterize the isoform of NOS present in oxyntic mucosa. Oxyntic mucosal segments from rat stomach were stained

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8

ROCZNIAK, AGNES, JAMES N. FRYER, DAVID Z. LEVINE, and KEVIN D. BURNS. "Downregulation of Neuronal Nitric Oxide Synthase in the Rat Remnant Kidney." Journal of the American Society of Nephrology 10, no. 4 (April 1999): 704–13. http://dx.doi.org/10.1681/asn.v104704.

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Abstract. Chronic renal failure is associated with disturbances in nitric oxide (NO) production. This study was conducted to determine the effect of 5/6 nephrectomy (5/6 Nx) on expression of intrarenal neuronal nitric oxide synthase (nNOS) in the rat. In normal rat kidney, nNOS protein was detected in the macula densa and in the cytoplasm and nuclei of cells of the inner medullary collecting duct by both immunofluorescence and electron microscopy. Western blot analysis revealed that 2 wk after 5/6 Nx, there were significant decreases in nNOS protein expression in renal cortex (sham: 95.42 ± 15

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9

Wang, Xianhong, Ming Lu, Yongzong Gao, Andreas Papapetropoulos, William C. Sessa, and Wenhui Wang. "Neuronal nitric oxide synthase is expressed in principal cell of collecting duct." American Journal of Physiology-Renal Physiology 275, no. 3 (September 1, 1998): F395—F399. http://dx.doi.org/10.1152/ajprenal.1998.275.3.f395.

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We used the RT-PCR technique and immunocytochemical methods to determine the expression of endothelial nitric oxide synthase (eNOS) or neuronal nitric oxide synthase (nNOS) in the cortical collecting duct (CCD) in rats on high-K+ diet. The microdissected CCDs of the rat kidney were lysed, and RT-PCR was carried out using rat nNOS and eNOS gene-specific primers. Southern analysis showed the presence of mRNA of nNOS but not eNOS in the CCD. The presence of nNOS in the CCD was further confirmed by light microscopy. We used the polyclonal nNOS antibody in immunocytochemical studies of the isolated

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10

Smith, Cheryl A., Beth Santymire, Aaron Erdely, Vasuki Venkat, György Losonczy, and Chris Baylis. "Renal nitric oxide production in rat pregnancy: role of constitutive nitric oxide synthases." American Journal of Physiology-Renal Physiology 299, no. 4 (October 2010): F830—F836. http://dx.doi.org/10.1152/ajprenal.00300.2010.

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Functional studies show that increased renal nitric oxide (NO) mediates the renal vasodilation and increased glomerular filtration rate that occur during normal pregnancy. We investigated whether changes in the constitutive NO synthases (NOS), endothelial (eNOS) and neuronal (nNOS), were associated with the increased renal NO production in normal midterm pregnancy in the rat. In kidneys from midterm pregnant (MP: 11–13 days gestation), late-term pregnant (LP: 18–20 days gestation), and similarly aged virgin (V) rats, transcript and protein abundance for eNOS and the nNOSα and nNOSβ splice vari

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11

Browne, Susan E., Cenk Ayata, Paul L. Huang, Michael A. Moskowitz, and M. Flint Beal. "The Cerebral Metabolic Consequences of Nitric Oxide Synthase Deficiency: Glucose Utilization in Endothelial and Neuronal Nitric Oxide Synthase Null Mice." Journal of Cerebral Blood Flow & Metabolism 19, no. 2 (February 1999): 144–48. http://dx.doi.org/10.1097/00004647-199902000-00005.

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Nitric oxide has multiple physiologic roles in the CNS. Inhibiting nitric oxide synthesis might therefore alter functional activity within the brain. We used [14C]-2-deoxyglucose in vivo autoradiography to measure local CMRglc in “knockout” mice lacking the genes for either the endothelial (eNOS) or neuronal (nNOS) isoforms of nitric oxide synthase, and in the progenitor strains (SV129, CS7B1/6). Glucose utilization levels did not significantly differ between nNOS and eNOS knockout mice and C57B1/6 mice in any of the 48 brain regions examined, but were relatively lower in some subcortical regi

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12

Ichihara, Atsuhiro, Edward W. Inscho, John D. Imig, and L. Gabriel Navar. "Neuronal nitric oxide synthase modulates rat renal microvascular function." American Journal of Physiology-Renal Physiology 274, no. 3 (March 1, 1998): F516—F524. http://dx.doi.org/10.1152/ajprenal.1998.274.3.f516.

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This study was performed to determine the influence of neuronal nitric oxide synthase (nNOS) on renal arteriolar tone under conditions of normal, interrupted, and increased volume delivery to the macula densa segment and on the microvascular responses to angiotensin II (ANG II). Experiments were performed in vitro on afferent (21.2 ± 0.2 μm) and efferent (18.5 ± 0.2 μm) arterioles of kidneys harvested from male Sprague-Dawley rats, using the blood-perfused juxtamedullary nephron technique. Superfusion with the specific nNOS inhibitor, S-methyl-l-thiocitrulline (l-SMTC), decreased afferent and

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13

Song, Tao, Katsuyoshi Sugimoto, Hideshi Ihara, Akihiro Mizutani, Naoya Hatano, Kodai Kume, Toshie Kambe, Fuminori Yamaguchi, Masaaki Tokuda, and Yasuo Watanabe. "p90 RSK-1 associates with and inhibits neuronal nitric oxide synthase." Biochemical Journal 401, no. 2 (December 21, 2006): 391–98. http://dx.doi.org/10.1042/bj20060580.

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Evidence is presented that RSK1 (ribosomal S6 kinase 1), a downstream target of MAPK (mitogen-activated protein kinase), directly phosphorylates nNOS (neuronal nitric oxide synthase) on Ser847 in response to mitogens. The phosphorylation thus increases greatly following EGF (epidermal growth factor) treatment of rat pituitary tumour GH3 cells and is reduced by exposure to the MEK (MAPK/extracellular-signal-regulated kinase kinase) inhibitor PD98059. Furthermore, it is significantly enhanced by expression of wild-type RSK1 and antagonized by kinase-inactive RSK1 or specific reduction of endogen

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14

CAO, LUXIANG, and WILLIAM D. ELDRED. "Subcellular localization of neuronal nitric oxide synthase in turtle retina: Electron immunocytochemistry." Visual Neuroscience 18, no. 6 (November 2001): 949–60. http://dx.doi.org/10.1017/s0952523801186128.

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Recent studies imaging nitric oxide (NO) production in the retina have indicated a much wider distribution of NO production than would be suggested by previous light-microscopic localizations of neuronal nitric oxide synthase (nNOS). To help resolve this discrepancy, the present study analyzed the ultrastructural localization of nNOS-like immunoreactivity (-LI) in all layers of the retina. In the ellipsoids of rod photoreceptors and the accessory elements of double cones, nNOS-LI was associated with some atypical mitochondria. In the outer plexiform layer, nNOS-LI was in some postsynaptic hori

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15

van’t Hof, Robert J., Jeny MacPhee, Helene Libouban, Miep H. Helfrich, and Stuart H. Ralston. "Regulation of Bone Mass and Bone Turnover by Neuronal Nitric Oxide Synthase." Endocrinology 145, no. 11 (November 1, 2004): 5068–74. http://dx.doi.org/10.1210/en.2004-0205.

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Abstract Nitric oxide (NO) is produced by NO synthase (NOS) and plays an important role in the regulation of bone cell function. The endothelial NOS isoform is essential for normal osteoblast function, whereas the inducible NOS isoform acts as a mediator of cytokine effects in bone. The role of the neuronal isoform of NOS (nNOS) in bone has been studied little thus far. Therefore, we investigated the role of nNOS in bone metabolism by studying mice with targeted inactivation of the nNOS gene. Bone mineral density (BMD) was significantly higher in nNOS knockout (KO) mice compared with wild-type

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Sears, Claire E., Euan A. Ashley, and Barbara Casadei. "Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?" Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1446 (June 29, 2004): 1021–44. http://dx.doi.org/10.1098/rstb.2004.1477.

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Nitric oxide (NO) has been shown to regulate cardiac function, both in physiological conditions and in disease states. However, several aspects of NO signalling in the myocardium remain poorly understood. It is becoming increasingly apparent that the disparate functions ascribed to NO result from its generation by different isoforms of the NO synthase (NOS) enzyme, the varying subcellular localization and regulation of NOS isoforms and their effector proteins. Some apparently contrasting findings may have arisen from the use of non–isoform–specific inhibitors of NOS, and from the assumption th

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Stewart, Julian M., Marvin S. Medow, Christopher T. Minson, and Indu Taneja. "Cutaneous neuronal nitric oxide is specifically decreased in postural tachycardia syndrome." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (October 2007): H2161—H2167. http://dx.doi.org/10.1152/ajpheart.00600.2007.

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Low flow postural tachycardia syndrome (POTS), is associated with reduced nitric oxide (NO) activity assumed to be of endothelial origin. We tested the hypothesis that cutaneous microvascular neuronal NO (nNO) is impaired, rather than endothelial NO (eNO), in POTS. We performed three sets of experiments on subjects aged 22.5 ± 2 yr. We used laser-Doppler flowmetry response to sequentially increase acetylcholine (ACh) doses and the local cutaneous heating response of the calf as bioassays for NO. During local heating we showed that when the selective neuronal nNO synthase (nNOS) inhibitor Nω-ni

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Zhang, Yin Hua. "Nitric oxide signalling and neuronal nitric oxide synthase in the heart under stress." F1000Research 6 (May 23, 2017): 742. http://dx.doi.org/10.12688/f1000research.10128.1.

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Nitric oxide (NO) is an imperative regulator of the cardiovascular system and is a critical mechanism in preventing the pathogenesis and progression of the diseased heart. The scenario of bioavailable NO in the myocardium is complex: 1) NO is derived from both endogenous NO synthases (endothelial, neuronal, and/or inducible NOSs [eNOS, nNOS, and/or iNOS]) and exogenous sources (entero-salivary NO pathway) and the amount of NO from exogenous sources varies significantly; 2) NOSs are located at discrete compartments of cardiac myocytes and are regulated by distinctive mechanisms under stress; 3)

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Li, Huiying, Joumana Jamal, Carla Plaza, Stephanie Hai Pineda, Georges Chreifi, Qing Jing, Maris A. Cinelli, Richard B. Silverman, and Thomas L. Poulos. "Structures of human constitutive nitric oxide synthases." Acta Crystallographica Section D Biological Crystallography 70, no. 10 (September 27, 2014): 2667–74. http://dx.doi.org/10.1107/s1399004714017064.

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Mammals produce three isoforms of nitric oxide synthase (NOS): neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). The overproduction of NO by nNOS is associated with a number of neurodegenerative disorders; therefore, a desirable therapeutic goal is the design of drugs that target nNOS but not the other isoforms. Crystallography, coupled with computational approaches and medicinal chemistry, has played a critical role in developing highly selective nNOS inhibitors that exhibit exceptional neuroprotective properties. For historic reasons, crystallography has focused on rat nN

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HUANG, PAUL L. "Mouse Models of Nitric Oxide Synthase Deficiency." Journal of the American Society of Nephrology 11, suppl 2 (November 2000): S120—S123. http://dx.doi.org/10.1681/asn.v11suppl_2s120.

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Abstract. Knockout mice for each of the three nitric oxide (NO) synthase (NOS) genes have been generated. Their phenotypes reflect the roles of each NOS isoform in physiologic and pathologic processes. This article reviews how neuronal NOS (nNOS) and endothelial NOS (eNOS) knockout mice have contributed to our knowledge of the roles of NO in cerebral ischemia, cardiovascular processes, and the autonomic nervous system. In some instances, the effects of NO produced by one isoform antagonize the effects of NO produced by another isoform. For example, after cerebral ischemia, the nNOS isoform is

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Xu, Lieming, Ethan P. Carter, Mamiko Ohara, Pierre-Yves Martin, Boris Rogachev, Kenneth Morris, Melissa Cadnapaphornchai, Mladen Knotek, and Robert W. Schrier. "Neuronal nitric oxide synthase and systemic vasodilation in rats with cirrhosis." American Journal of Physiology-Renal Physiology 279, no. 6 (December 1, 2000): F1110—F1115. http://dx.doi.org/10.1152/ajprenal.2000.279.6.f1110.

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Cirrhosis is typically associated with a hyperdynamic circulation consisting of low blood pressure, low systemic vascular resistance (SVR), and high cardiac output. We have recently reported that nonspecific inhibition of nitric oxide synthase (NOS) with nitro-l-arginine methyl ester reverses the hyperdynamic circulation in rats with advanced liver cirrhosis induced by carbon tetrachloride (CCl4). Although an important role for endothelial NOS (eNOS) is documented in cirrhosis, the role of neuronal NOS (nNOS) has not been investigated. The present study was carried out to specifically investig

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Saur, Dieter, Winfried L. Neuhuber, Bernd Gengenbach, Andrea Huber, Volker Schusdziarra, and Hans-Dieter Allescher. "Site-specific gene expression of nNOS variants in distinct functional regions of rat gastrointestinal tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 2 (February 1, 2002): G349—G358. http://dx.doi.org/10.1152/ajpgi.00226.2001.

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5′ mRNA variants of neuronal nitric oxide synthase (nNOS) are generated either by alternative promoter usage resulting in different mRNAs that encode for the same protein (nNOSα) or alternative splicing encoding NH2-terminally truncated proteins (nNOSβ/γ) that lack the PDZ/GLGF domain for protein-protein interaction of nNOSα. We studied the expression of 5′ nNOS mRNA forms and nNOS-interacting proteins (postsynaptic density protein-95; PSD-95) in the rat gastrointestinal tract and analyzed the more distinct localization of nNOS protein variants in the duodenum by immunohistochemistry with COOH

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Battish, Raman, Gao-Yuan Cao, Richard B. Lynn, Sushanta Chakder, and Satish Rattan. "Heme oxygenase-2 distribution in anorectum: colocalization with neuronal nitric oxide synthase." American Journal of Physiology-Gastrointestinal and Liver Physiology 278, no. 1 (January 1, 2000): G148—G155. http://dx.doi.org/10.1152/ajpgi.2000.278.1.g148.

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Recent investigations have suggested carbon monoxide (CO) as a putative messenger molecule. Although several studies have implicated the heme oxygenase (HO) pathway, responsible for the endogenous production of CO, in the neuromodulatory control of the internal anal sphincter (IAS), its exact role is not known. Nitric oxide, produced by neuronal nitric oxide synthase (nNOS) of myenteric neurons, is an important inhibitory neural messenger molecule mediating nonadrenergic noncholinergic (NANC) relaxation of the IAS. The present studies were undertaken to investigate in detail the presence and c

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Staunton, Michael, Cathy Drexler, Phillip G. Schmid, Heather S. Havlik, Antal G. Hudetz, and Neil E. Farber. "Neuronal Nitric Oxide Synthase Mediates Halothane-induced Cerebral Microvascular Dilation." Anesthesiology 92, no. 1 (January 1, 2000): 125. http://dx.doi.org/10.1097/00000542-200001000-00023.

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Background The causes of volatile anesthetic-induced cerebral vasodilation include direct effects on smooth muscle and indirect effects via changes in metabolic rate and release of mediators from vascular endothelium and brain parenchyma. The role of nitric oxide and the relative importance of neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively) are unclear. Methods Rat brain slices were superfused with oxygenated artificial cerebrospinal fluid. Hippocampal arteriolar diameters were measured using computerized videomicrometry. Vessels were preconstricted with prostaglan

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VALLON, VOLKER, TIMOTHY TRAYNOR, LUCIANO BARAJAS, YUNING G. HUANG, JOSIE P. BRIGGS, and JÜRGEN SCHNERMANN. "Feedback Control of Glomerular Vascular Tone in Neuronal Nitric Oxide Synthase Knockout Mice." Journal of the American Society of Nephrology 12, no. 8 (August 2001): 1599–606. http://dx.doi.org/10.1681/asn.v1281599.

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Abstract. For further elucidation of the role of neuronal nitric oxide synthase (nNOS) in macula densa (MD) cells, experiments were performed in anesthetized nNOS knockout mice (nNOS -/-). At comparable levels of arterial BP, renal blood flow was not significantly different between nNOS +/+ and nNOS -/- (1.7 ± 0.2 versus 1.4 ± 0.1 ml/min), and autoregulation of renal blood flow was maintained to a pressure level of approximately 85 mmHg in both groups of mice (n = 6 in each group). The fall in proximal tubular stop-flow pressure in response to an increase in loop of Henle perfusion rate from 0

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Guerra, Damian D., Rachael Bok, Vibhuti Vyas, David J. Orlicky, Ramón A. Lorca, and K. Joseph Hurt. "Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum." Proceedings of the National Academy of Sciences 116, no. 35 (August 12, 2019): 17541–46. http://dx.doi.org/10.1073/pnas.1905902116.

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Nitric oxide (NO) is a major inhibitory neurotransmitter that mediates nonadrenergic noncholinergic (NANC) signaling. Neuronal NO synthase (nNOS) is activated by Ca2+/calmodulin to produce NO, which causes smooth muscle relaxation to regulate physiologic tone. nNOS serine1412 (S1412) phosphorylation may reduce the activating Ca2+ requirement and sustain NO production. We developed and characterized a nonphosphorylatable nNOSS1412A knock-in mouse and evaluated its enteric neurotransmission and gastrointestinal (GI) motility to understand the physiologic significance of nNOS S1412 phosphorylatio

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Roczniak, Agnes, David Z. Levine, and Kevin D. Burns. "Localization of protein inhibitor of neuronal nitric oxide synthase in rat kidney." American Journal of Physiology-Renal Physiology 278, no. 5 (May 1, 2000): F702—F707. http://dx.doi.org/10.1152/ajprenal.2000.278.5.f702.

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We have recently demonstrated that in rats with 5/6 nephrectomy (5/6 Nx), renal cortical and inner medullary neuronal NOS (nNOS) expression is downregulated, associated with decreased urinary excretion of nitric oxide (NO) products. Recently, a novel 89-amino acid protein [protein inhibitor of nNOS (PIN)] was isolated from rat brain and shown to inhibit nNOS activity. The present studies localized PIN in the rat kidney and determined the effect of 5/6 Nx on PIN expression. By RT-PCR, PIN mRNA was detected in the kidney cortex and inner medulla. Immunohistochemistry revealed staining for PIN in

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Okamoto, Hirotsugu, Wei Meng, Jinya Ma, Cenk Ayata, Richard J. Roman, Zeljko J. Bosnjak, John P. Kampine, Paul L. Huang, Michael A. Moskowitz, and Antal G. Hudetz. "Isoflurane-induced Cerebral Hyperemia in Neuronal Nitric Oxide Synthase Gene Deficient Mice." Anesthesiology 86, no. 4 (April 1, 1997): 875–84. http://dx.doi.org/10.1097/00000542-199704000-00018.

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Background Nitric oxide (NO) has been reported to play an important role in isoflurane-induced cerebral hyperemia in vivo. In the brain, there are two constitutive isoforms of NO synthase (NOS), endothelial NOS (eNOS), and neuronal NOS (nNOS). Recently, the mutant mouse deficient in nNOS gene expression (nNOS knockout) has been developed. The present study was designed to examine the role of the two constitutive NOS isoforms in cerebral blood flow (CBF) response to isoflurane using this nNOS knockout mouse. Methods Regional CBF (rCBF) in the cerebral cortex was measured with laser-Doppler flow

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Pelletier, Anne-Marie, Shriram Venkataramana, Kurtis G. Miller, Brian M. Bennett, Dileep G. Nair, Sandra Lourenssen, and Michael G. Blennerhassett. "Neuronal nitric oxide inhibits intestinal smooth muscle growth." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 6 (June 2010): G896—G907. http://dx.doi.org/10.1152/ajpgi.00259.2009.

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Hyperplasia of smooth muscle contributes to the thickening of the intestinal wall that is characteristic of inflammation, but the mechanisms of growth control are unknown. Nitric oxide (NO) from enteric neurons expressing neuronal NO synthase (nNOS) might normally inhibit intestinal smooth muscle cell (ISMC) growth, and this was tested in vitro. In ISMC from the circular smooth muscle of the adult rat colon, chemical NO donors inhibited [3H]thymidine uptake in response to FCS, reducing this to baseline without toxicity. This effect was inhibited by the guanylyl cyclase inhibitor ODQ and potent

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CAO, QI-LIN, HEATHER A. MURPHY, and HEYWOOD M. PETRY. "Localization of nitric oxide synthase in the tree shrew retina." Visual Neuroscience 16, no. 3 (May 1999): 399–409. http://dx.doi.org/10.1017/s0952523899163016.

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Nitric oxide (NO) is a novel neuronal messenger that likely influences retinal function by activating retinal guanylyl cyclase to increase levels of cGMP. In the present study, the localization of neuronal nitric oxide synthase (nNOS, Type I NOS) in the cone-dominant tree shrew retina was studied using NADPH-d histochemistry and nNOS immunocytochemistry. Both NADPH-d and nNOS-immunoreactivity (IR) labeled the inner segments of rods and the myoids of a regular subpopulation of cones, with their corresponding nuclei outlined. The labeled cone myoids were co-localized with a marker for short-wave

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Nakada, Satoshi, Yuri Yamashita, Shuichi Machida, Yuko Miyagoe-Suzuki, and Eri Arikawa-Hirasawa. "Perlecan Facilitates Neuronal Nitric Oxide Synthase Delocalization in Denervation-Induced Muscle Atrophy." Cells 9, no. 11 (November 23, 2020): 2524. http://dx.doi.org/10.3390/cells9112524.

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Perlecan is an extracellular matrix molecule anchored to the sarcolemma by a dystrophin–glycoprotein complex. Perlecan-deficient mice are tolerant to muscle atrophy, suggesting that perlecan negatively regulates mechanical stress-dependent skeletal muscle mass. Delocalization of neuronal nitric oxide synthase (nNOS) from the sarcolemma to the cytosol triggers protein degradation, thereby initiating skeletal muscle atrophy. We hypothesized that perlecan regulates nNOS delocalization and activates protein degradation during this process. To determine the role of perlecan in nNOS-mediated mechano

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Caggiano, Anthony O., and Richard P. Kraig. "Neuronal Nitric Oxide Synthase Expression is Induced in Neocortical Astrocytes after Spreading Depression." Journal of Cerebral Blood Flow & Metabolism 18, no. 1 (January 1998): 75–87. http://dx.doi.org/10.1097/00004647-199801000-00008.

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Spreading depression (SD) confers either increased susceptibility to ischemic injury or a delayed protection. Because nitric oxide modulates ischemic injury, we investigated if altered expression of nitric oxide synthase (NOS) by SD could account for the effect of SD on ischemia. Furthermore, the identity of cells expressing NOS after SD is important, since SD results in heterogeneous, cell type–specific changes in intracellular environment, which can control NOS activity. Immunohistochemical, computer-based image analyses and Western blotting show that the number of neuronal NOS (nNOS)–positi

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Takata, Tsuyoshi, Shoma Araki, Yukihiro Tsuchiya, and Yasuo Watanabe. "Oxidative Stress Orchestrates MAPK and Nitric-Oxide Synthase Signal." International Journal of Molecular Sciences 21, no. 22 (November 19, 2020): 8750. http://dx.doi.org/10.3390/ijms21228750.

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Reactive oxygen species (ROS) are not only harmful to cell survival but also essential to cell signaling through cysteine-based redox switches. In fact, ROS triggers the potential activation of mitogen-activated protein kinases (MAPKs). The 90 kDa ribosomal S6 kinase 1 (RSK1), one of the downstream mediators of the MAPK pathway, is implicated in various cellular processes through phosphorylating different substrates. As such, RSK1 associates with and phosphorylates neuronal nitric oxide (NO) synthase (nNOS) at Ser847, leading to a decrease in NO generation. In addition, the RSK1 activity is se

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Donato, Jose, Renata Frazão, Makoto Fukuda, Claudia R. Vianna, and Carol F. Elias. "Leptin Induces Phosphorylation of Neuronal Nitric Oxide Synthase in Defined Hypothalamic Neurons." Endocrinology 151, no. 11 (September 29, 2010): 5415–27. http://dx.doi.org/10.1210/en.2010-0651.

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Studies have indicated that the neurotransmitter nitric oxide (NO) mediates leptin’s effects in the neuroendocrine reproductive axis. However, the neurons involved in these effects and their regulation by leptin is still unknown. We aimed to determine whether NO neurons are direct targets of leptin and by which mechanisms leptin may influence neuronal NO synthase (nNOS) activity. Nicotinamide adenine dinucleotide phosphate diaphorase activity and leptin-induced phosphorylation of signal transducer and activator of transcription-3 immunoreactivity were coexpressed in subsets of neurons of the m

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Ihara, Hideshi, Yousuke Inui, Tomoaki Ida, Tomohiro Sawa, Yasuo Watanabe та Takaaki Akaike. "P90. Superoxide production by neuronal nitric oxide synthase (nNOS)-α and nNOS-μ". Nitric Oxide 19 (2008): 64. http://dx.doi.org/10.1016/j.niox.2008.06.188.

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Wood, Michael W., Richard C. Hastings, and Linda A. Sygowski. "A Homogeneous Fluorescent Cell-Based Assay for Detection of Heterologously Expressed Nitric Oxide Synthase Activity." Journal of Biomolecular Screening 10, no. 8 (October 18, 2005): 849–55. http://dx.doi.org/10.1177/1087057105280640.

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Arhodamine-derived, membrane-permeable fluorophore (DAR-4MAM) sensitive to nitric oxide production has been developed recently. The authors evaluated this reagent in both 96 and 384-well formats using heterologously expressed neuronal nitric oxide synthase (nNOS). nNOS transfected into HEK-293T cellswas stimulated by the addition of ionomycin. The calcium mobilization resulting from ionomycin treatment of nNOS-expressing 293T cells induced a robust increase in emission intensity, as measured using a standard rhodamine filter set. The effect was time dependent, and a 3 to 4-fold stimulation cou

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Abram, S. R., B. T. Alexander, W. A. Bennett, and J. P. Granger. "Role of neuronal nitric oxide synthase in mediating renal hemodynamic changes during pregnancy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 5 (November 1, 2001): R1390—R1393. http://dx.doi.org/10.1152/ajpregu.2001.281.5.r1390.

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Renal plasma flow (RPF) and glomerular filtration rate (GFR) are markedly increased during pregnancy. We recently reported that the renal hemodynamic changes observed during pregnancy in rats are associated with enhanced renal protein expression of neuronal nitric oxide synthase (nNOS). The purpose of this study was to determine the role of nNOS in mediating renal hemodynamic changes observed during pregnancy. To achieve this goal, we examined the effects of the nNOS inhibitor 7-nitroindazole (7-NI) on kidney function in normal conscious, chronically instrumented virgin ( n = 6) and pregnant r

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Araki, Shoma, Koji Osuka, Tsuyoshi Takata, Yukihiro Tsuchiya, and Yasuo Watanabe. "Coordination between Calcium/Calmodulin-Dependent Protein Kinase II and Neuronal Nitric Oxide Synthase in Neurons." International Journal of Molecular Sciences 21, no. 21 (October 27, 2020): 7997. http://dx.doi.org/10.3390/ijms21217997.

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Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is highly abundant in the brain and exhibits broad substrate specificity, thereby it is thought to participate in the regulation of neuronal death and survival. Nitric oxide (NO), produced by neuronal NO synthase (nNOS), is an important neurotransmitter and plays a role in neuronal activity including learning and memory processes. However, high levels of NO can contribute to excitotoxicity following a stroke and neurodegenerative disease. Aside from NO, nNOS also generates superoxide which is involved in both cell injury and signaling.

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Premaratne, Shyamal, John M. McCarty, Robert W. McCuen, Pam M. Malone, Bruno Neu, Wolfgang Schepp, Chun Xue, and Mitchell L. Schubert. "Neuronal nitric oxide synthase (NNOS): Expression in rat parietal cells." Gastroenterology 118, no. 4 (April 2000): A32. http://dx.doi.org/10.1016/s0016-5085(00)82196-4.

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Carvalho, Tais H. F., Oswaldo U. Lopes, and Fatima R. Tolentino-Silva. "Baroreflex responses in neuronal nitric oxide synthase knoukout mice (nNOS)." Autonomic Neuroscience 126-127 (June 2006): 163–68. http://dx.doi.org/10.1016/j.autneu.2006.03.001.

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SONG, Yao, Jay L. ZWEIER, and Yong XIA. "Heat-shock protein 90 augments neuronal nitric oxide synthase activity by enhancing Ca2+/calmodulin binding." Biochemical Journal 355, no. 2 (April 6, 2001): 357–60. http://dx.doi.org/10.1042/bj3550357.

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Heat-shock protein 90 (hsp90) has been shown to facilitate neuronal NO synthase (nNOS, type 1) activity in vivo. But the direct effect of hsp90 on purified nNOS has not been determined yet. Moreover, the mechanism underlying the action of hsp90 is not known. nNOS activity is primarily initiated and regulated by the binding of Ca2+/calmodulin (CaM). Therefore, we explored whether hsp90 modulates nNOS activity by affecting CaM binding. Recombinant rat nNOS was purified from the stably transfected cells by affinity chromatography. hsp90 increased nNOS activity in a dose-dependent manner with an E

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Katakam, Prasad V. G., Somhrita Dutta, Venkata N. Sure, Samuel M. Grovenburg, Angellica O. Gordon, Nicholas R. Peterson, Ibolya Rutkai, and David W. Busija. "Depolarization of mitochondria in neurons promotes activation of nitric oxide synthase and generation of nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 9 (May 1, 2016): H1097—H1106. http://dx.doi.org/10.1152/ajpheart.00759.2015.

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The diverse signaling events following mitochondrial depolarization in neurons are not clear. We examined for the first time the effects of mitochondrial depolarization on mitochondrial function, intracellular calcium, neuronal nitric oxide synthase (nNOS) activation, and nitric oxide (NO) production in cultured neurons and perivascular nerves. Cultured rat primary cortical neurons were studied on 7–10 days in vitro, and endothelium-denuded cerebral arteries of adult Sprague-Dawley rats were studied ex vivo. Diazoxide and BMS-191095 (BMS), activators of mitochondrial KATP channels, depolarized

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Gamé, Xavier, Julien Allard, Ghislaine Escourrou, Pierre Gourdy, Ivan Tack, Pascal Rischmann, Jean-François Arnal, and Bernard Malavaud. "Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 3 (March 2008): R851—R857. http://dx.doi.org/10.1152/ajpregu.00467.2007.

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Estrogens are known to modulate lower urinary tract (LUT) trophicity and neuronal nitric oxide synthase (nNOS) expression in several organs. The aim of this study was to explore the effects of endogenous and supraestrus levels of 17β-estradiol (E2) on LUT and urethral nNOS expression and function. LUT function and histology and urethral nNOS expression were studied in adult female mice subjected either to sham surgery, surgical castration, or castration plus chronic E2 supplementation (80 μg·kg−1·day−1, i.e., pregnancy level). The micturition pattern was profoundly altered by long-term supraes

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Capettini, L. S. A., S. F. Cortes, M. A. Gomes, G. A. B. Silva, J. L. Pesquero, M. J. Lopes, M. M. Teixeira, and V. S. Lemos. "Neuronal nitric oxide synthase-derived hydrogen peroxide is a major endothelium-dependent relaxing factor." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 6 (December 2008): H2503—H2511. http://dx.doi.org/10.1152/ajpheart.00731.2008.

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Endothelium-dependent vasorelaxation in large vessels is mainly attributed to Nω-nitro-l-arginine methyl ester (l-NAME)-sensitive endothelial nitric oxide (NO) synthase (eNOS)-derived NO production. Endothelium-derived hyperpolarizing factor (EDHF) is the component of endothelium-dependent relaxations that resists full blockade of NO synthases (NOS) and cyclooxygenases. H2O2 has been proposed as an EDHF in resistance vessels. In this work we propose that in mice aorta neuronal (n)NOS-derived H2O2 accounts for a large proportion of endothelium-dependent ACh-induced relaxation. In mice aorta rin

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Reiser, Peter J., William O. Kline, and Pal L. Vaghy. "Induction of neuronal type nitric oxide synthase in skeletal muscle by chronic electrical stimulation in vivo." Journal of Applied Physiology 82, no. 4 (April 1, 1997): 1250–55. http://dx.doi.org/10.1152/jappl.1997.82.4.1250.

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Reiser, Peter J., William O. Kline, and Pal L. Vaghy.Induction of neuronal type nitric oxide synthase in skeletal muscle by chronic electrical stimulation in vivo. J. Appl. Physiol. 82(4): 1250–1255, 1997.—Fast-twitch skeletal muscles contain more neuronal-type nitric oxide synthase (nNOS) than slow-twitch muscles because nNOS is present only in fast (type II) muscle fibers. Chronic in vivo electrical stimulation of tibialis anterior and extensor digitorum longus muscles of rabbits was used as a method of inducing fast-to-slow fiber type transformation. We have studied whether an increase in m

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Bandyopadhyay, A., S. Chakder, and S. Rattan. "Regulation of inducible and neuronal nitric oxide synthase gene expression by interferon-gamma and VIP." American Journal of Physiology-Cell Physiology 272, no. 6 (June 1, 1997): C1790—C1797. http://dx.doi.org/10.1152/ajpcell.1997.272.6.c1790.

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The studies examined the regulation of inducible and neuronal nitric oxide synthases (iNOS and nNOS, respectively) in the rat brain, stomach, rectum, and spleen. Relative expression of iNOS and nNOS mRNAs was quantified by the sensitive method of polymerase amplification reactions. The NOS proteins were determined by Western blot, using specific antibodies. Highest levels of nNOS and iNOS mRNAs were expressed in the rat brain and spleen, respectively. Furthermore, both nNOS and iNOS were expressed in the stomach and rectum. Interestingly, treatment of tissues with lipopolysaccharides or cytoki

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Song, Yao, Jay L. Zweier, and Yong Xia. "Determination of the enhancing action of HSP90 on neuronal nitric oxide synthase by EPR spectroscopy." American Journal of Physiology-Cell Physiology 281, no. 6 (December 1, 2001): C1819—C1824. http://dx.doi.org/10.1152/ajpcell.2001.281.6.c1819.

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Recent studies showed that heat shock protein 90 (HSP90) enhances nitric oxide (NO) synthesis from endothelial and neuronal NO synthase (eNOS and nNOS, respectively). However, these findings were based on indirect NO measurements. Moreover, although our previous studies showed that the action of HSP90 involves increased Ca2+/calmodulin (Ca2+/CaM) binding, quantitative measurements of the effect of HSP90 on CaM binding to nNOS have been lacking. With electron paramagnetic resonance spectroscopy, we directly measured NO signals from purified nNOS. HSP90 augmented NO formation from nNOS in a dose

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Lekontseva, Olga, Yanyan Jiang, Caitlyn Schleppe, and Sandra T. Davidge. "Altered Neuronal Nitric Oxide Synthase in the Aging Vascular System: Implications for Estrogens Therapy." Endocrinology 153, no. 8 (June 14, 2012): 3940–48. http://dx.doi.org/10.1210/en.2012-1071.

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Ovarian dysfunction at any age is associated with increased cardiovascular risk in women; however, therapeutic effects of exogenous estrogens are age dependent. Estradiol (E2) activates neuronal nitric oxide synthase (nNOS) in vascular cells. Because nNOS is prone to uncoupling under unfavorable biochemical conditions (as seen in aging), E2 stimulation of nNOS may lack vascular benefits in aging. Small mesenteric arteries were isolated from female Sprague Dawley rats, 3 or 12 months old, who were ovariectomized (Ovx) and treated with placebo or E2 for 4 wk. Vascular relaxation to exogenous E2

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Lefer, David J., Steven P. Jones, Wesley G. Girod, Amarpreet Baines, Matthew B. Grisham, Adam S. Cockrell, Paul L. Huang, and Rosario Scalia. "Leukocyte-endothelial cell interactions in nitric oxide synthase-deficient mice." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1943—H1950. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1943.

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Nitric oxide (NO) is known to be an important endogenous modulator of leukocyte-endothelial cell interactions within the microcirculation. We examined leukocyte rolling and adhesion under baseline conditions and following thrombin (0.25 U/ml) superfusion in the mesentery of wild-type, inducible NOS (iNOS)-deficient (−/−), neuronal NOS (nNOS) −/−, and endothelial cell NOS (ecNOS) −/− mice to further our understanding of NO and leukocyte function. Baseline leukocyte rolling (cells/min) was significantly elevated in both the nNOS −/− (30.0 ± 4.0) and ecNOS −/− mice (67.0 ± 12.0) compared with wil

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Chetty, C. S., G. R. Reddy, K. S. Murthy, J. Johnson, K. Sajwan, and D. Desaiah. "Perinatal Lead Exposure Alters the Expression of Neuronal Nitric Oxide Synthase in Rat Brain." International Journal of Toxicology 20, no. 3 (May 2001): 113–20. http://dx.doi.org/10.1080/109158101317097692.

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Environmental exposure to lead (Pb) is known to affect the developing nervous system causing cognitive deficits in children. The diffusible nitric oxide (NO) is a biological messenger known to be involved in brain development. We examined the developmental changes of neuronal nitric oxide synthase (nNOS) in cerebellum and hippocampus of developing rat brain by radiometric assay, Western blot analysis and immunohistochemistry. Pb-exposure (0.2% Pb acetate) was initiated on gestation day 6 through the drinking water of the dam and continued through birth and postnatal days (PNDs) 1 to 21. The pu

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