Nitric Oxide

There has been an explosive increase in the amount of interesting information about the physiologic and pathophysiologic roles of nitric oxide in cardiovascular, nervous, and immune systems. The possible involvement of the nitric oxide-cyclic guanosine monophosphate pathway in the effects of anesthetic agents has been the focus of many investigators. Relaxations of cerebral and peripheral arterial smooth muscle as well as increases in cerebral and other regional blood flows induced by anesthetic agents are mediated mainly via nitric oxide released from the endothelium and/or the nitrergic nerve and also via prostaglandin I2 or endothelium-derived hyperpolarizing factor. Preconditioning with volatile anesthetics protects against ischemia-reperfusion-induced myocardial dysfunction and cell death or neurotoxicity, possibly through nitric oxide release. Inhibition of nitric oxide synthase decreases the anesthetic requirement. Involvement of nitric oxide in the effects of volatile, intravenous, and local anesthetics differs. This review article includes a summary of information about the sites and mechanisms by which various anesthetic agents interact with the nitric oxide-cyclic guanosine monophosphate system.

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Vulgarenol, a Sesquiterpene Isolated from Magnolia grandiflora, Induces Nitric Oxide Synthases II and III Overexpression in Guinea Pig Hearts

Zeitschrift für Naturforschung C ◽

10.1515/znc-2007-9-1016 ◽

2007 ◽

Vol 62 (9-10) ◽

pp. 725-730 ◽

Cited By ~ 4

Author(s):

Leonardo del Valle-Mondragón ◽

Fermín Alejandro Tenorio-López ◽

Gabriela Zarco-Olvera ◽

Gustavo Pastelín-Hernández

Keyword(s):

Nitric Oxide ◽

Soluble Guanylyl Cyclase ◽

Cyclic Guanosine Monophosphate ◽

Guanosine Monophosphate ◽

Control Group ◽

Perfused Heart ◽

Vasodilator Effect ◽

Nitric Oxide Release ◽

Magnolia Grandiflora ◽

Coronary Vasodilator

Vulgarenol, a sesquiterpene isolated from Magnolia grandiflora flower petals, decreased coronary vascular resistance in the Langendorff isolated and perfused heart model, when compared to the control group [(15.2 × 107 ± 1.0 × 107) dyn s cm-5 vs. (36.8 X 107 ± 1.2 × 107) dyn s cm-5]. Our data suggest that this coronary vasodilator effect probably involved inducible and endothelial nitric oxide synthase overexpression (6.8 and 4.2 times over control, respectively), which correlated with increases in nitric oxide release [(223 ± 9) pmol mL-1 vs. (61 ±11) pmol mL-1] and in cyclic guanosine monophosphate production [(142 ± 8) pmol mg-1 of tissue vs. (44±10) pmol mg-1 of tissue], as compared to control values. This effect was antagonized by 3 μm gadolinium(III) chloride, 100 μm N-nitro-L-arginine methyl ester, and 10 μm 1H-[1,2,4]oxadiazolo[4,2-a]quinoxalin-1-one. Hence, the vulgarenol-elicited coronary vasodilator effect could be mediated by the nitric oxide-soluble guanylyl cyclase pathway.

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Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin in Clione limacina Central Pattern Generator Swim Interneurons

Integrative Organismal Biology ◽

10.1093/iob/obaa045 ◽

2020 ◽

Author(s):

Thomas J Pirtle ◽

Richard A Satterlie

Keyword(s):

Nitric Oxide ◽

Central Pattern Generator ◽

Guanylyl Cyclase ◽

Signal Transduction Pathway ◽

Soluble Guanylyl Cyclase ◽

Cyclic Guanosine Monophosphate ◽

Pattern Generator ◽

Guanosine Monophosphate ◽

Cellular Changes ◽

Clione Limacina

Abstract Typically, the marine mollusk, Clione limacina, exhibits a slow, hovering locomotor gait to maintain its position in the water column. However, the animal exhibits behaviorally relevant locomotor swim acceleration during escape response and feeding behavior. Both nitric oxide and serotonin mediate this behavioral swim acceleration. In this study, we examine the role that the second messenger, cGMP, plays in mediating nitric oxide and serotonin-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of soluble guanylyl cyclase decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in Clione. Because nitric oxide has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in Clione swim interneurons that are consistent with cellular changes produced by serotonin application, we hypothesize that both nitric oxide and serotonin function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates nitric oxide-induced but not serotonin-induced swim acceleration in Clione.

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The nitric oxide–cGMP signaling pathway plays a significant role in tolerance to the analgesic effect of morphine

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y10-109 ◽

2011 ◽

Vol 89 (2) ◽

pp. 89-95 ◽

Cited By ~ 22

Author(s):

Ercan Ozdemir ◽

Ihsan Bagcivan ◽

Nedim Durmus ◽

Ahmet Altun ◽

Sinan Gursoy

Keyword(s):

Nitric Oxide ◽

Analgesic Effect ◽

Soluble Guanylate Cyclase ◽

Morphine Tolerance ◽

Cyclic Guanosine Monophosphate ◽

Guanosine Monophosphate ◽

Albino Rats ◽

Tail Flick ◽

Analgesic Effects ◽

Cgmp Signaling

Although the phenomenon of opioid tolerance has been widely investigated, neither opioid nor nonopioid mechanisms are completely understood. The aim of the present study was to investigate the role of the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway in the development of morphine-induced analgesia tolerance. The study was carried out on male Wistar albino rats (weighing 180–210 g; n = 126). To develop morphine tolerance, animals were given morphine (50 mg/kg; s.c.) once daily for 3 days. After the last dose of morphine was injected on day 4, morphine tolerance was evaluated. The analgesic effects of 3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole (YC-1), BAY 41-2272, S-nitroso-N-acetylpenicillamine (SNAP), NG-nitro-l-arginine methyl ester (L-NAME), and morphine were considered at 15 or 30 min intervals (0, 15, 30, 60, 90, and 120 min) by tail-flick and hot-plate analgesia tests (n = 6 in each study group). The results showed that YC-1 and BAY 41-2272, a NO-independent activator of soluble guanylate cyclase (sGC), significantly increased the development and expression of morphine tolerance, and L-NAME, a NO synthase (NOS) inhibitor, significantly decreased the development of morphine tolerance. In conclusion, these data demonstrate that the nitric oxide–cGMP signal pathway plays a pivotal role in developing tolerance to the analgesic effect of morphine.

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Nitric Oxide/Cyclic Guanosine Monophosphate Signalling Mediates an Inhibitory Action on Sensory Pathways of the Micturition Reflex in the Rat

European Urology ◽

10.1016/j.eururo.2010.07.026 ◽

2010 ◽

Vol 58 (4) ◽

pp. 616-625 ◽

Cited By ~ 46

Author(s):

Romain Caremel ◽

Stephanie Oger-Roussel ◽

Delphine Behr-Roussel ◽

Philippe Grise ◽

François A. Giuliano

Keyword(s):

Nitric Oxide ◽

Inhibitory Action ◽

Cyclic Guanosine Monophosphate ◽

Guanosine Monophosphate ◽

Micturition Reflex ◽

Sensory Pathways

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Breathing nitric oxide plus hydrogen gas reduces ischemia-reperfusion injury and nitrotyrosine production in murine heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00844.2012 ◽

2013 ◽

Vol 305 (4) ◽

pp. H542-H550 ◽

Cited By ~ 22

Author(s):

Toshihiro Shinbo ◽

Kenichi Kokubo ◽

Yuri Sato ◽

Shintaro Hagiri ◽

Ryuji Hataishi ◽

...

Keyword(s):

Nitric Oxide ◽

Cardiac Function ◽

Infarct Size ◽

Ischemia Reperfusion Injury ◽

Myocardial Dysfunction ◽

Ischemia Reperfusion ◽

Neutrophil Infiltration ◽

Left Ventricular ◽

Hydrogen Gas ◽

Coronary Artery Ligation

Inhaled nitric oxide (NO) has been reported to decrease the infarct size in cardiac ischemia-reperfusion (I/R) injury. However, reactive nitrogen species (RNS) produced by NO cause myocardial dysfunction and injury. Because H2 is reported to eliminate peroxynitrite, it was expected to reduce the adverse effects of NO. In mice, left anterior descending coronary artery ligation for 60 min followed by reperfusion was performed with inhaled NO [80 parts per million (ppm)], H2 (2%), or NO + H2, starting 5 min before reperfusion for 35 min. After 24 h, left ventricular function, infarct size, and area at risk (AAR) were assessed. Oxidative stress associated with reactive oxygen species (ROS) was evaluated by staining for 8-hydroxy-2′-deoxyguanosine and 4-hydroxy-2-nonenal, that associated with RNS by staining for nitrotyrosine, and neutrophil infiltration by staining for granulocyte receptor-1. The infarct size/AAR decreased with breathing NO or H2 alone. NO inhalation plus H2 reduced the infarct size/AAR, with significant interaction between the two, reducing ROS and neutrophil infiltration, and improved the cardiac function to normal levels. Although nitrotyrosine staining was prominent after NO inhalation alone, it was eliminated after breathing a mixture of H2 with NO. Preconditioning with NO significantly reduced the infarct size/AAR, but not preconditioning with H2. In conclusion, breathing NO + H2 during I/R reduced the infarct size and maintained cardiac function, and reduced the generation of myocardial nitrotyrosine associated with NO inhalation. Administration of NO + H2 gases for inhalation may be useful for planned coronary interventions or for the treatment of I/R injury.

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Direct measurement of nitric oxide release in gastric mucosa during ischemia-reperfusion in rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.274.3.g465 ◽

1998 ◽

Vol 274 (3) ◽

pp. G465-G471 ◽

Cited By ~ 9

Author(s):

Kouichirou Wada ◽

Yoshinori Kamisaki ◽

Tsuyoshi Ohkura ◽

Gaku Kanda ◽

Kentaro Nakamoto ◽

...

Keyword(s):

Nitric Oxide ◽

Gastric Mucosa ◽

Superoxide Radical ◽

Ischemia Reperfusion ◽

Mucosal Injury ◽

Celiac Artery ◽

Radical Scavenger ◽

Gastric Mucosal Lesions ◽

Nitric Oxide Release ◽

Pentobarbital Sodium Anesthesia

Nitric oxide (NO) generation in the rat gastric mucosa during ischemia-reperfusion was measured using an NO-sensitive electrode. Under pentobarbital sodium anesthesia, an electrode was inserted into the submucosa from the serous membrane side in the fundus. After steady-state baseline recording, the celiac artery was clamped for 30 min, and then ischemia-reperfusion was achieved by removing the clamp. The clamping of the celiac artery caused a decrease in blood flow and an increase in NO level in the gastric tissue. Just after the removal of the clamp, the NO level rapidly fell and returned to the baseline level. Administration of N G-nitro-l-arginine methyl ester (an NO synthase inhibitor, 30 mg/kg ip) before ischemia significantly attenuated both the increase in NO level during ischemia and the formation of acute gastric mucosal lesions observed after 60 min reperfusion. Administration of superoxide dismutase (a superoxide radical scavenger, 10,000 U/kg iv) at the end of ischemia inhibited both the rapid decrease in NO level during the reperfusion and the gastric mucosal erosions. Because NO and superoxide radical produce a highly reactive peroxynitrite, it can be argued that NO has an important pathological role in acute gastric mucosal injury induced by ischemia-reperfusion. Our conclusion was strongly supported by immunohistochemical staining of nitrotyrosine residues, an indication of peroxynitrite formation.

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