Home About us Contact
|
Home About us Contact | ||
|
|
||
NO Formation (no + formation)
Selected AbstractsNerve growth factor increases airway responses and decreases levels of exhaled nitric oxide during histamine challenge in an in vivo guinea-pig modelACTA PHYSIOLOGICA, Issue 2 2001S. G. Friberg There is a growing body of evidence supporting the idea that nerve growth factor (NGF) may be involved in the development of asthma-associated symptoms, such as airway hyper-responsiveness. Increased levels of NGF have recently been described in serum and in the airways of asthmatics. We have examined whether exhaled nitric oxide (NO) levels might be altered during the increased airway responses upon NGF treatment in guinea-pigs in vivo. Intravenous (i.v.) administration of histamine normally elicits a rapid peak in insufflation pressure (IP) and in exhaled NO, followed by a period of decreased concentrations of exhaled NO. Anaesthetized guinea-pigs were pre-treated intravenously with either saline, 4 or 80 ng kg,1 NGF 30 min before i.v. challenge with 16 ,g kg,1 histamine. At 80 ng kg,1 NGF significantly enhanced the airway obstruction caused by histamine, whereas the peak acute increase in exhaled NO was not enhanced. Following the increase, came a rapid drop, an effect enforced in the NGF treated animals. Subsequently, the time to return to 90% of resting exhaled NO was increased, from 12 min in saline-treated animals to 48 min in NGF-treated animals. Our data confirm that NGF can enhance airway responses to histamine. Moreover, our study shows a decrease in exhaled NO following a histamine challenge, an effect enhanced by NGF. A reduced ability to release exhaled NO may be a mechanism for increased airway responses during elevated NGF levels. The interaction between NGF and airway NO formation, and its relation to airway responses, merit further investigation. [source] Numerical study on NO formation in CH4,O2,N2 diffusion flame diluted with CO2INTERNATIONAL JOURNAL OF ENERGY RESEARCH, Issue 2 2005Dong-Jin Hwang Abstract Numerical study with momentum-balanced boundary conditions has been conducted to grasp chemical effects of added CO2, to either fuel- or oxidizer-side on flame structure and NO emission behaviour in CH4,O2,N2 diffusion flames. Cautious investigation is made for the comparison among the behaviours of principal chain branching and important H-removal key reactions. This describes successfully the reason why flame temperatures for fuel-side dilution are higher than those for oxidizer-side dilution. The role of the principal chain branching reaction is also recognized to be important even in the change of major flame structure caused by chemical effects. The importantly contributing reaction steps to NO production are examined. The reduced production rates of thermal NO and prompt NO due to chemical effects are much more remarkable for fuel-side dilution. It is also found that the reaction step, H+NO+M=HNO+M plays a decisive role of the formation and destruction of prompt NO. Copyright © 2005 John Wiley & Sons, Ltd. [source] Numerical study on flame structure and NO formation in CH4,O2,N2 counterflow diffusion flame diluted with H2OINTERNATIONAL JOURNAL OF ENERGY RESEARCH, Issue 14 2004Dong-Jin Hwang Abstract Numerical study on flame structure and NO emission behaviour has been conducted to grasp chemical effects of added H2O on either fuel- or oxidizer-side in CH4,O2,N2 counterflow diffusion flames. An artificial species, which has the same thermodynamic, transport, and radiation properties of added H2O, is introduced to feasibly isolate the chemical effects. Special concern is focused on the important role of remarkably produced OH radicals due to chemical effects of added H2O on flame structure and NO emission. The reason why the difference of behaviours between the principal chain branching reaction rate and flame temperature appear is attributed to the drastic change of reaction step (R120) from the production to the consumption of OH. It is also, however, seen that the most important contribution of produced OH due to chemical effects of added H2O is through reaction step (R127). The importantly contributing reaction steps to NO production are also examined. The production rates of thermal NO and prompt NO are suppressed by chemical effects of added H2O. The contribution of the reaction steps related to HNO intermediate species to the production of prompt NO is also stressed. Copyright © 2004 John Wiley & Sons, Ltd. [source] Characterization of signaling pathway for the translocation of neuronal nitric oxide synthase to the plasma membrane by PACAPJOURNAL OF NEUROCHEMISTRY, Issue 6 2008Takayuki Ohnishi Abstract In the central nervous system, the activation of neuronal nitric oxide synthase (nNOS) is closely associated with activation of NMDA receptor, and trafficking of nNOS may be a prerequisite for efficient NO production at synapses. We recently demonstrated that pituitary adenylate cyclase activating polypeptide (PACAP) and NMDA synergistically caused the translocation of nNOS to the membrane and stimulated NO production in PC12 (pheochromocytoma) cells. However, the mechanisms responsible for trafficking and activation of nNOS are largely unknown. To address these issues, here we constructed a yellow fluorescent protein (YFP)-tagged nNOS N-terminal (1,299 a.a.) mutant, nNOSNT-YFP, and visualized its translocation in PC12 cells stably expressing it. PACAP enhanced the translocation synergistically with NMDA in a time- and concentration-dependent manner. The translocation was blocked by inhibitors of protein kinase A (PKA), protein kinase C (PKC), and Src kinase; and the effect of PACAP could be replaced with PKA and PKC activators. The ,-finger region in the PSD-95/disc large/zonula occludens-1 domain of nNOS was required for the translocation of nNOS and its interaction with post-synaptic density-95 (PSD-95), and NO formation was attenuated by dominant negative nNOSNT-YFP. These results demonstrate that PACAP stimulated nNOS translocation mediated by PKA and PKC via PAC1 -receptor (a PACAP receptor) and suggest cross-talk between PACAP and NMDA for nNOS activation by Src-dependent phosphorylation of NMDA receptors. [source] Melatonin protects against streptozotocin, but not interleukin-1,-induced damage of rodent pancreatic ,-cellsJOURNAL OF PINEAL RESEARCH, Issue 3 2001Annika K. Andersson In the present study, we examined whether melatonin can protect rodent pancreatic islets against streptozotocin (STZ) and interleukin-1, (IL-1,)-induced suppression of ,-cell function. Formation of free radicals, DNA damage and extensive DNA repair leading to depletion of intracellular nicotinamide adenine dinucleotide (NAD) may mediate STZ toxicity. Activation of inducible nitric oxide synthase and nitric oxide (NO) formation may cause IL-1,-induced ,-cell impairment. We also studied the effect of melatonin against STZ-induced hyperglycemia in C57BL/Ks mice. For in vitro studies, cultured rat islets were exposed to melatonin (100 ,M,1 mM) 30 min prior to STZ (0.5 mM) or IL-1, (25 U/mL) addition. After an additional 30 min incubation with STZ, islet function and NAD content were analyzed either acutely or after 18 hr of recovery in fresh culture medium. For IL-1, experiments, islets were incubated for 48 hr with the cytokine before evaluation of islet function. We found that melatonin counteracted STZ-induced inhibition of glucose metabolism and insulin release in cultured rat islets after 18 hr of recovery. Moreover, NAD levels were higher in the melatonin-treated group at this time point. Melatonin had no effect on IL-1,-induced islet inhibition of glucose oxidation or NO formation. Diabetes induced by STZ (140 mg/kg body weight; i.v.) was effectively prevented by administration of melatonin (100 mg/kg body weight; i.p.) 30 min before STZ injection. We conclude that the protective effects of melatonin against ,-cell damage may be related to interference with DNA damage and poly(ADP-ribose) polymerase (PARP) activation rather than through effects on NO generation pathways. [source] Extracellular Arginine Rapidly Dilates In Vivo Intestinal Arteries and Arterioles Through a Nitric Oxide MechanismMICROCIRCULATION, Issue 2 2008Laura Pezzuto ABSTRACT Objective: Arginine used for nitric oxide formation can be from intracellular stores or transported into cells. The study evaluated the rapidity, and primary site of NO and vascular resistance responses to arginine at near physiological concentrations (100,400 , M). Methods: Arginine was applied to a single arteriole through a micropipette to determine the fastest possible responses. For vascular blood flow and [NO] responses, arginine was added to the bathing media. Results: Dilation of single arterioles to arginine began in 10,15 seconds and application over the entire vasculature increased [NO] in , 60,90 seconds, and flow increased within 120,300 seconds. Resting periarteriolar [NO] for arterioles was 493.6 ± 30.5 nM and increased to 696.1 ± 68.2 and 820.1 ± 110.5 nM at 200 and 400 , M L-arginine. The blood flow increased 50% at 400,1200 , M L-arginine. The reduced arterial resistance during topical arginine was significantly greater than microvascular resistance at 100 and 200 , M arginine. All responses were blocked by L-NAME. Conclusions: This study demonstrated arterial resistance responses are as or more responsive to arginine induced NO formation as arterioles at near physiological concentrations of arginine. The vascular NO and resistance responses occurred rapidly at L-arginine concentrations at and below 400 , M, which predict arginine transport processes were involved. [source] 2223: Carbon monoxide as a mediator in the retinaACTA OPHTHALMOLOGICA, Issue 2010C BUCOLO Purpose Carbonic monoxide (CO) is organic gas ubiquitously synthesized in mammalian tissues by enzyme that has constitutive and inducible forms. This gas is produced as metabolic end-product in specific cell life phases, and may acts as atypical neuronal messenger. Evidence has recently accumulated suggesting that CO may be cytoprotective because its bioactions, including inhibition of apoptosis, platelet aggregation, complement activation, and inflammatory cytokine production. CO appears to be important to counteract the cytotoxicity caused by excessive production of reactive oxygen (ROS) and nitrogen (RNS) species. Methods In vitro and in vivo models. Results Induction of heme oxygenase (HO)-1 by hemin has been found to prevent retinal cell death after ischemia provoked by ocular hypertension in rats. The LPS-induced expression of pro-inflammatory cytokines, in rat eye, is also inhibited by CO. Interestingly, drugs active as inhibitors of iNOS block CO-induced increases in cGMP in the retina.Drugs inhibiting NO formation by acting on iNOS activity have been found to potently reduce intraocular pressure. Studies from our lab showed that an increase of CO availability by hemin or carbon monoxide-releasing molecules lower the intraocular pressure, suggesting a suppress action of iNOS-derived NO production. Conclusion A better understanding of CO regulation may lead to new therapeutic options that are safer and more efficacious than currently available treatments for various sight-threatening eye diseases, such as retinal degenerations. [source] Multiple Mechanisms Of Early Hyperglycaemic Injury Of The Rat Intestinal MicrocirculationCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2002H Glenn Bohlen SUMMARY 1. Hyperglycaemia in the vast majority of humans with diabetes mellitus is the end result of profound insulin resistance secondary to obesity. For patients in treatment, hyperglycaemia is usually not sustained but, rather, occurs intermittently. In in vivo studies of the rat intestinal microcirculation, endothelial impairment occurs within 30 min at D -glucose concentrations , 300 mg/dL. Endothelial-dependent dilation to acetylcholine and constriction to noradrenaline is impaired. Vasodilation to exogenous nitric oxide (NO) remains normal. 2. When initiated before hyperglycaemia, suppression of oxygen radicals by both scavenging and pretreatment with cyclo-oxygenase blockade to prevent oxygen radical formation minimized endothelial impairments during hyperglycaemia. Neither treatment was effective in restoring endothelial function once it was damaged by hyperglycaemia. 3. A mechanism that may initiate the arachidonic acid, oxygen radical process is activation of specific isoforms of protein kinase C (PKC). De novo formation of diacylglycerol during hyperglycaemia activates PKC. Blockade of the ,II PKC isoform with LY-333531 prior to hyperglycaemia protected NO formation within the arteriolar wall, as judged with NO-sensitive microelectrodes. Furthermore, once suppression of endothelial dilation was present in untreated animals, PKC blockade could substantially restore endothelial-dependent dilation. 4. These results indicate that acute hyperglycaemia is far from benign and, in the rat, causes rapid endothelial impairment. Both oxygen radical scavenging and cyclo-oxygenase blockade prior to bouts of hyperglycaemia minimize endothelial impairment with limited side effects. Blockade of specific PKC isozymes protects endothelial function both as a pre- or post-treatment during moderately severe hyperglycaemia. [source] | |||||||||||||