Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q8IXL6 (RNS)
 1,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of atrial natriuretic factor (ANF) on neural control of renin release and sodium excretion by the kidney were examined in pentobarbital-anesthetized dogs. Electrical stimulation of the renal nerves (RNS, 1 Hz) increased the renal secretion rate of renin (RSR) by 627 +/- 141 ng angiotensin I (ANG I)/min and that of norepinephrine (NESR) by 22.2 +/- 5.9 ng/min. Furthermore, urinary sodium excretion (UNaV) was decreased by 59 +/- 7%, with little change in either renal blood flow (RBF) or glomerular filtration rate (GFR). Intrarenal arterial infusion of ANF (alpha-human atrial natriuretic peptide; 10 ng.kg-1.min-1) increased basal UNaV about twofold but had no effect on basal RBF or GFR. The RNS-induced increase in RSR during ANF infusion (198 +/- 117 ng ANG I/min) was significantly lower than that before the infusion (P less than 0.05), whereas the RNS-induced changes in NESR (27.1 +/- 8.5 ng/min) and UNaV (51 +/- 11%) were unaffected. These results suggest that neural stimulation of renin release, but not of tubular sodium reabsorption, can be suppressed by exogenously administered ANF at a dose that does not affect glomerular filtration or renal neurotransmitter release.
Am J Physiol 1989 Sep
PMID:Atrial natriuretic factor suppresses neural stimulation of renin release in dogs. 257 Dec 99

We compared changes in amplitude and area of surface recorded compound motor action potentials (CMAPs) during 20-Hz repetitive nerve stimulation and after maximum voluntary contraction in patients with the Lambert-Eaton myasthenic syndrome (LEMS), myasthenia gravis (MG), and normal controls. There was greater potentiation of CMAP amplitude after voluntary contraction than during 20-Hz stimulation in 10 of 14 LEMS patients; CMAP area increased more after exercise than during 20-Hz stimulation in all LEMS patients. Although abnormal potentiation of CMAP area and amplitude was seen in equal numbers of LEMS patients, more LEMS patients demonstrated a greater than 100% potentiation of CMAP area than of CMAP amplitude. We conclude that maximum voluntary contraction is preferable to brief 20-Hz RNS to demonstrate potentiation in LEMS because it is at least as sensitive and is less painful. Measurement of CMAP area in LEMS patients is not better than measuring the change in CMAP amplitude in demonstrating abnormal potentiation. Testing of a single hand muscle for potentiation in LEMS does not demonstrate abnormal potentiation in all LEMS patients.
Muscle Nerve 1994 Sep
PMID:Repetitive nerve stimulation studies in the Lambert-Eaton myasthenic syndrome. 750 83

A 54-year-old neurotic patient developed pyridostigmine-induced proximal weakness with daily 3600 mg of pyridostigmine. Detailed analysis of the RNS test showed three different types of responses which were reproduced in the in vitro nerve-muscle preparation, confirming that three different responses represent the different degree of pyridostigmine toxicity. One of responses was a pattern, thought to be typical of anticholinesterase toxicity: repetitive discharge and the maximal decrement in the second response followed by an increment (dip phenomenon). With reduction of pyridostigmine, clinical and electrophysiological improvement followed.
Electromyogr Clin Neurophysiol 1993 Sep
PMID:Pyridostigmine toxicity. Electrophysiological study. 822 30

Previous studies on patients with breast cancer, who received postsurgical irradiation, displayed a markedly suppressed inflammatory response in the lung of smoking patients compared to nonsmokers. The aim of the present study was to investigate further the effect of exposure to tobacco smoke on the development of irradiation-induced pneumonitis in the rat. Four groups of animals were used: controls (C); those exposed to tobacco smoke (S); those irradiated but not exposed to smoke (RNS); and those irradiated and exposed to tobacco smoke (RS). The rats were exposed to a diluted main stream of cigarette smoke, at a concentration of about 0.4 mg.l-1, in a nose-only exposure system for 1 h.day-1, 5 days.week-1 for 10 weeks. Exposure to tobacco smoke started 3 weeks before irradiation. The basal one third of both lungs was exposed to a single radiation dose of 28 Gy (6 MeV photons). All animals were killed 7 weeks after irradiation. We compared findings in bronchoalveolar lavage (BAL) and tissue morphology. The alveolar tissue showed less inflammation in the RS-group than in the RNS-group. Most strikingly, mast cells were increased one hundredfold in the lung interstitium and thirty fold in the peribronchial area in the RNS-group, whereas no increase was found in the RS-group or in the controls. The alveolar septa of the RNS-group were thickened, with occurrence of inflammatory cells and mast cells, whereas the RS-group displayed no difference as compared to the non-irradiated, nonsmoking group (C).(ABSTRACT TRUNCATED AT 250 WORDS)
Eur Respir J 1993 Sep
PMID:Tobacco smoke exposure suppresses radiation-induced inflammation in the lung: a study of bronchoalveolar lavage and ultrastructural morphology in the rat. 822 33

Neuropeptide Y (NPY) is a 36-amino acid peptide that is colocalized and released with norepinephrine (NE) from central and peripheral adrenergic neurons and has been suggested to contribute to the control of vascular tone. This study was undertaken to assess the contribution of NPY at the vascular adrenergic neuroeffector junction in the rat kidney. Experiments were performed in isolated rat kidneys prelabeled with tritiated NE ([3H] NE). Infusion of NPY (1-50 nM) resulted in a dose-dependent increase in basal perfusion pressure and potentiated the vasoconstrictor response elicited by renal nerve stimulation (RNS; 0.5-4 Hz). NPY (10-50 nM) also potentiated the vasoconstrictor response elicited by exogenous NE (150 pmol). These effects of NPY were mimicked by [Leu31,Pro34]NPY, a NPY Y1 receptor agonist whereas [13-36]NPY, a NPY Y2 receptor agonist failed to alter the basal, RNS- or NE-induced increase in perfusion pressure. NPY (10 nM) and [Leu31,Pro34]NPY but not [13-36] NPY inhibited RNS-induced fractional tritium overflow only at high frequencies of stimulation (10 and 16 Hz) without altering basal tritium efflux. Periarterial nerve stimulation at 4 and 10 Hz resulted in release of immunoreactive NPY by 8- and 38-fold, respectively. These data indicate that NPY acts primarily at the postjunctional sites to produce renal vasoconstriction and to potentiate the vasoconstrictor response to RNS via Y1 receptors. Furthermore, NPY coreleased with adrenergic transmitter may also inhibit release of NE at higher frequencies of RNS (8-16 Hz) by acting on Y1 receptors at the prejunctional sites.
J Pharmacol Exp Ther 1993 Sep
PMID:Neuropeptide Y modulates the vascular response to periarterial nerve stimulation primarily by a postjunctional action in the isolated perfused rat kidney. 837 Nov 40

Epidemiologic and occupational studies indicate adverse health effects due to inhalation of particulate air pollutants, but precise biologic mechanisms responsible have yet to be fully established. The tracheobronchial epithelium forms the body's first physiologic barrier to such airborne pollutants, where ciliary movement functions to remove the offending substances caught in the overlying mucus layer. Resident and infiltrating phagocytic cells also function in this removal process. In this paper, we examine the role of reactive oxygen and nitrogen species (ROS/RNS) in the response of airway epithelium to particulates. Some particulates themselves can generate ROS, as can the epithelial cells, in response to appropriate stimulation. In addition, resident macrophages in the airways and the alveolar spaces can release ROS/RNS after phagocytosis of inhaled particles. These macrophages also release large amounts of tumor necrosis factor alpha (TNF-alpha), a cytokine that can generate responses within the airway epithelium dependent upon intracellular generation of ROS/RNS. As a result, signal transduction pathways are set in motion that may contribute to inflammation and other pathobiology in the airway. Such effects include increased expression of intercellular adhesion molecule 1, interleukin-6, cytosolic and inducible nitric oxide synthase, manganese superoxide dismutase, cytosolic phospholipase A2, and hypersecretion of mucus. Ultimately, ROS/RNS may play a role in the global response of the airway epithelium to particulate pollutants via activation of kinases and transcription factors common to many response genes. Thus, defense mechanisms involved in responding to offending particulates may result in a complex cascade of events that can contribute to airway pathology.
Environ Health Perspect 1997 Sep
PMID:The role of reactive oxygen and nitrogen species in the response of airway epithelium to particulates. 940 Jul 42

Peroxynitrite (ONOO-) is a strong oxidant derived from nitric oxide ('NO) and superoxide (O2.-), reactive nitrogen (RNS) and oxygen species (ROS) present in inflamed tissue. Other oxidant stresses, e.g., TNF-alpha and hyperoxia, induce mitochondrial, manganese-containing superoxide dismutase (MnSOD) gene expression. These experiments tested whether ONOO regulated MnSOD gene expression in human lung epithelial (A549) cells. 3-morpholinosydnonimine HCI (SIN-1) (10 or 1000 microM) increased MnSOD mRNA, but did not change hypoxanthine guanine phosphoribosyl transferase (HPRT) mRNA. Authentic peroxynitrite (ONOO ) (100-500 microM) also increased MnSOD mRNA but did not change constitutive HPRT mRNA expression. ONOO stimulated luciferase gene expression driven by a 2.5 kb fragment of the rat MnSOD gene 5' promoter region. MnSOD gene induction due to ONOO- was inhibited effectively by L-cysteine (10 mM) and partially inhibited by N-acetyl cysteine (50 mM) or pyrrole dithiocarbamate (10 mM). .NO from 1-propanamine, 3-(2-hydroxy-2-nitroso-1-propylhydrazine) (PAPA NONOate) (100 or 1000 microM) did not change MnSOD or HPRT mRNA. Neither H202 nor NO2-, breakdown products of SIN-1 and ONOO , had any effect on MnSOD mRNA expression; however, ONOO- and SIN-1 did not increase MnSOD protein content detectable by western blots, nor did they increase MnSOD enzymatic activity. Increased steady state [O2.-] in the presence of .NO yields ONOO , and ONOO has direct, stimulatory effects on MnSOD transcript expression.
Free Radic Biol Med 1998 Sep
PMID:Peroxynitrite modulates MnSOD gene expression in lung epithelial cells. 974 82

The ISIAH rat strain with stress-sensitive arterial hypertension was intentionally selected to study the role of stress as a factor in the development of arterial hypertension. This study aimed to determine the role of reactive oxygen and nitrogen species (ROS and RNS) in the pathogenesis of hypertension in ISIAH rats. The nitric oxide concentrations measured by EPR were found to be significantly higher for hypertensive ISIAH rats compared with that for normotensive Wistar rats in both the aortic wall (2 times) and cerebellum (1.5 times). The activity of superoxide dismutase measured in the blood of ISIAH rats was found to be about 1.5 times lower compared with that of Wistar rats. These data support the suggestion that ROS and RNS, including superoxide radicals and nitric oxide, may play an important role in development of stress-induced hypertension in ISIAH rats. The tissue content of reduced thiols has been considered as a marker of oxidative damage. To study the tissue oxidative status we used an EPR method for quantitative determination of SH groups. The concentration of reduced thiols in the blood of ISIAH rats was much lower than that in Wistar rats (0.6 +/- 0.05 and 1.57 +/- 0.1 mM, respectively).
Biochem Biophys Res Commun 1999 Sep 24
PMID:Manifestation of oxidative stress in the pathogenesis of arterial hypertension in ISIAH rats. 1049 14

Methamphetamine (METH) produces dopaminergic neurotoxicity by the production of reactive oxygen (ROS) and nitrogen (RNS) species. The role of free radicals has also been implicated in the process of aging. The present study was designed to evaluate whether METH-induced dopaminergic neurotoxicity and hyperthermia is a result of peroxynitrite production and if these effects correlate with age. One-, six- and 12-month-old male rats (n = 8) were administered a single dose of METH (0, 5, 10, 20, and 40 mg/kg, intraperitoneally). The formation of 3-nitrotyrosine (3-NT) as a marker of peroxynitrite production as well as dopamine and its metabolites DOPAC and HVA were measured in the striatum 4-h after METH-administration. Rectal temperature was monitored every 30 min after METH administration until 4 h. At 40 mg/kg METH, a 100% mortality in 12-month-old animals was observed, whereas no deaths occurred in 1- or 6-month-old rats. An age-dependent increase in hyperthermia was observed after METH-administration. A similar pattern of dose-dependent increase in the formation of 3-NT and in the depletion of dopamine and its metabolites with age was observed in the striatum. Furthermore, no effect was observed at 5 mg/kg METH in 1-month-old animals, whereas the effect was significant in 6- and 12-month-old animals. These data suggest that aging increases the susceptibility of the animals toward METH-induced peroxynitrite generation and striatal dopaminergic neurotoxicity.
J Neurochem 2001 Sep
PMID:Aging increases the susceptiblity to methamphetamine-induced dopaminergic neurotoxicity in rats: correlation with peroxynitrite production and hyperthermia. 1155 69

This study evaluates the action of the new ruthenium complexes trans-RuCl(2)(nic)(4)] (I) and trans-[RuCl(2)(i-nic)(4)] (II) as free radical scavengers. In our experiments, both compounds acted as scavengers of superoxide anion (O(2)*(-)), hydroxyl radicals (HO*) and nitrogen monoxide (formally known as 'nitric oxide'; NO*). In addition, complexes I and II potentiated the release of NO* from S-nitroso-N-acetyl-DL-penicilamine (SNAP), a NO* donor. Complex II, but not I, also decreased the nitrite levels in culture media of activated macrophages. A hypsochromic shift of lambda(max) and a significant change in half-wave potential (E(1/2)) was observed when NO* was added to the Complex II. Thiobarbituric reactive substance (TBARS) levels were significantly reduced in rats treated for 1 week with Complex II plus tert-butylhydroperoxide, when compared to rats treated only with tert-butylhydroperoxide. None of the complexes showed cytotoxicity. These findings support the suggestion that the new ruthenium complexes, especially trans-[RuCl(2)(i-nic)(4)] or its derivatives, might provide potential therapeutic benefits in disorders where reactive nitrogen (RNS) or oxygen (ROS) species are involved.
J Inorg Biochem 2001 Sep
PMID:Complexes trans-[RuCl(2)(nic)(4)] and trans-[RuCl(2)(i-nic)(4)] as free radical scavengers. 1156 31


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