Nasal Nitric Oxide Levels in Cystic Fibrosis Patients Are Associated with a Neuronal NO Synthase (NOS1) Gene Polymorphism

Nitric Oxide ◽  
2002 ◽  
Vol 6 (2) ◽  
pp. 236-241 ◽  
Author(s):  
H. Grasemann ◽  
K. Storm van's Gravesande ◽  
S. Gärtig ◽  
M. Kirsch ◽  
R. Büscher ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Gene Polymorphism ◽  
No Synthase ◽  
Neuronal No Synthase ◽  
Nasal Nitric Oxide

Influence of Atopy on Exhaled and Nasal Nitric Oxide in Cystic Fibrosis Patients

2008 ◽  
Vol 1 (1) ◽  
pp. 9-12
Author(s):  
R. Chiron ◽  
I. Vachier ◽  
F. Counil ◽  
P. Godard ◽  
P. Chanez
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Nasal Nitric Oxide

Nasal nitric oxide in cystic fibrosis with and without humming

2007 ◽  
Vol 37 (2) ◽  
pp. 140-144 ◽  
Author(s):  
V. M. D. Struben ◽  
W. V. Sewbalak ◽  
M. H. Wieringa ◽  
C. J. Mantingh ◽  
L. M. van den Toorn ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Nasal Nitric Oxide

scholarly journals Neuronal Nitric Oxide Synthase and Ischemia-Induced Neurogenesis

2005 ◽  
Vol 25 (4) ◽  
pp. 485-492 ◽  
Author(s):  
Yunjuan Sun ◽  
Kunlin Jin ◽  
Jocelyn T Childs ◽  
Lin Xie ◽  
Xiao Ou Mao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Selective Inhibition ◽  
No Synthase ◽  
Adult Brain ◽  
Brdu Incorporation ◽  
Neuronal No Synthase ◽  
Synthase Inhibitor

Nitric oxide (NO) influences infarct size after focal cerebral ischemia and also regulates neurogenesis in the adult brain. These observations suggest that therapeutic approaches to stroke that target NO signaling may provide neuroprotection and also enhance brain repair through cell replacement. However, ischemic injury and neurogenesis are both affected differently depending on which isoform of NO synthase is the source of NO. In addition, ischemia itself stimulates neurogenesis, and ischemia-induced neurogenesis may be regulated differently than neurogenesis in nonischemic brain. To determine how neuronal NO synthase affects ischemia-induced neurogenesis, transient focal cerebral ischemia was produced in wild-type mice and in knockout mice lacking neuronal NO synthase, and BrdU incorporation and doublecortin immunoreactivity were measured in the principal neuroproliferative regions of the adult brain. Knockout of neuronal NO synthase reduced infarct size and increased both basal and ischemia-induced neurogenesis, suggesting that NO from this source is an inhibitory regulator of neurogenesis in the ischemic brain. 7-Nitroindazole, an NO synthase inhibitor that preferentially affects the neuronal isoform, also increased neurogenesis in rats when administered by the intracerebroventricular route. Selective inhibition of neuronal NO synthase may have the potential to both reduce infarct size and enhance neurogenesis in stroke.

Resistance of PC12 cells against nitric oxide (NO)-induced toxicity in long-term culture: implication of neuronal NO synthase expression

2001 ◽  
Vol 309 (3) ◽  
pp. 169-172 ◽  
Author(s):  
Kohei Yuyama ◽  
Hideko Yamamoto ◽  
Kazuhiro Nakamura ◽  
Takeshi Kato ◽  
Ichiro Sora ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pc12 Cells ◽  
No Synthase ◽  
Neuronal No Synthase ◽  
Long Term Culture

scholarly journals Reduced Nasal Nitric Oxide Production in Cystic Fibrosis Patients with Elevated Systemic Inflammation Markers

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79141 ◽  
Author(s):  
Ruth K. Michl ◽  
Julia Hentschel ◽  
Christiane Fischer ◽  
James F. Beck ◽  
Jochen G. Mainz
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Systemic Inflammation ◽  
Nitric Oxide Production ◽  
Inflammation Markers ◽  
Oxide Production ◽  
Nasal Nitric Oxide

scholarly journals Blockade of neuronal nitric oxide synthase alters the baroreflex control of heart rate in the rabbit

1998 ◽  
Vol 274 (1) ◽  
pp. R181-R186 ◽  
Author(s):  
Hiroshi Murakami ◽  
Jun-Li Liu ◽  
Hirohito Yoneyama ◽  
Yasuhiro Nishida ◽  
Kenji Okada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
No Synthase ◽  
Baroreflex Control ◽  
Neuronal No Synthase ◽  
Significant Difference ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Oxide Synthase

In previous studies we used N G-nitro-l-arginine (l-NNA) to investigate the role of nitric oxide (NO) in baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA).l-NNA increased resting mean arterial pressure (MAP), decreased HR, and did not change or slightly decreased RSNA. These changes complicated the assessment of the central effects of NO on the baroreflex control of HR and RSNA. Therefore, in the present study the effects of the relatively selective neuronal NO synthase inhibitor 7-nitroindazole (7-NI) on the baroreflex control of HR and RSNA were investigated in rabbits. Intraperitoneal injection of 7-NI (50 mg/kg) had no effect on resting HR, MAP, or RSNA. 7-NI significantly reduced the lower plateau of the HR-MAP baroreflex curve from 140 ± 4 to 125 ± 4 and from 177 ± 10 to 120 ± 9 beats/min in conscious and anesthetized preparations, respectively ( P < 0.05). In contrast, there was no significant difference in the RSNA-MAP curves before and after 7-NI administration in conscious or anesthetized preparations. These data suggest that blockade of neuronal NO synthase influences baroreflex control of HR but not of RSNA in rabbits.

scholarly journals Nasal nitric oxide levels in primary ciliary dyskinesia, cystic fibrosis and healthy children

2019 ◽  
Vol 61 (1) ◽  
pp. 20
Author(s):  
Elif Güney ◽  
Nagehan Emiralioğlu ◽  
Güzin Cinel ◽  
Ebru Yalçın ◽  
Deniz Doğru ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Primary Ciliary Dyskinesia ◽  
Healthy Children ◽  
Nasal Nitric Oxide ◽  
Ciliary Dyskinesia

scholarly journals Suppression of Nitric Oxide (NO)-Dependent Behavior by Double-Stranded RNA-Mediated Silencing of a Neuronal NO Synthase Gene

2002 ◽  
Vol 22 (11) ◽  
pp. RC227-RC227 ◽  
Author(s):  
Sergei A. Korneev ◽  
Ildikó Kemenes ◽  
Volko Straub ◽  
Kevin Staras ◽  
Elena I. Korneeva ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
No Synthase ◽  
Double Stranded Rna ◽  
Neuronal No Synthase ◽  
Dependent Behavior

Preserved reflex cutaneous vasodilation in cystic fibrosis does not include an enhanced nitric oxide-dependent mechanism

2007 ◽  
Vol 102 (6) ◽  
pp. 2301-2306 ◽  
Author(s):  
Brad W. Wilkins ◽  
Elizabeth A. Martin ◽  
Shelly K. Roberts ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
No Synthase ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Reflex Cutaneous Vasodilation

In humans, vasoactive intestinal peptide (VIP) may play a role in reflex cutaneous vasodilation during body heating. We tested the hypothesis that the nitric oxide (NO)-dependent contribution to active vasodilation is enhanced in the skin of subjects with cystic fibrosis (CF), compensating for sparse levels of VIP. In 2 parallel protocols, microdialysis fibers were placed in the skin of 11 subjects with CF and 12 controls. Lactated Ringer was perfused at one microdialysis site and NG-nitro-l-arginine methyl ester (2.7 mg/ml) was perfused at a second microdialysis site. Skin blood flow was monitored over each site with laser-Doppler flowmetry. In protocol 1, local skin temperature was increased 0.5°C every 5 s to 42°C, and then it maintained at 42°C for ∼45 min. In protocol 2, subjects wore a tube-lined suit perfused with water at 50°C, sufficient to increase oral temperature (Tor) 0.8°C. Cutaneous vascular conductance (CVC) was calculated (flux/mean arterial pressure) and scaled as percent maximal CVC (sodium nitroprusside; 8.3 mg/ml). Vasodilation to local heating was similar between groups. The change (Δ%CVCmax) in CVC with NO synthase inhibition on the peak (9 ± 3 vs. 12 ± 5%CVCmax; P = 0.6) and the plateau (45 ± 3 vs. 35 ± 5%CVCmax; P = 0.1) phase of the skin blood flow response to local heating was similar in CF subjects and controls, respectively. Reflex cutaneous vasodilation increased CVC in CF subjects (58 ± 4%CVCmax) and controls (53 ± 4%CVCmax; P = 0.37) and NO synthase inhibition attenuated CVC in subjects with CF (37 ± 6%CVCmax) and controls (35 ± 5%CVCmax; P = 0.8) to a similar degree. Thus the preservation of cutaneous active vasodilation in subjects with CF is not associated with an enhanced NO-dependent vasodilation.

scholarly journals Nitric Oxide from Neuronal No-Synthase Increases after Beta-Adrenergic Stimulation but does not Control Mitochondrial Respiration in Cardiac Myocytes

2014 ◽  
Vol 106 (2) ◽  
pp. 184a-185a
Author(s):  
Michael Kohlhaas ◽  
Stefanie Bergem ◽  
Alexander Nickel ◽  
Maxie Meiser ◽  
Barbara Casadei ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Mitochondrial Respiration ◽  
No Synthase ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Neuronal No Synthase
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