Analysis of Nitric Oxide Synthase Genes in Cluster Headache

Cephalalgia ◽  
2002 ◽  
Vol 22 (9) ◽  
pp. 758-764 ◽  
Author(s):  
C Sjöstrand ◽  
H Modin ◽  
T Masterman ◽  
K Ekbom ◽  
E Waldenlind ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cluster Headache ◽  
Genetic Factors ◽  
International Headache Society ◽  
Critical Role ◽  
The Body ◽  
Control Group ◽  
Control Groups ◽  
Oxide Synthase ◽  
Pentanucleotide Repeat

The aetiology of cluster headache is still not yet completely understood, but the potential relevance of genetic factors has been recognized during recent years. Nitric oxide (NO) plays a critical role in the regulation of vasodilation, neurotransmission, inflammation and many other events throughout the body. NO also appears to be an important mediator of vascular headache pathophysiology. In this study we have performed an association analysis of five polymorphic micro-satellite markers in the three different NO synthase (NOS) genes; nNOS (NOS1), iNOS (NOS2A) and eNOS (NOS3). Ninety-one cluster headache patients diagnosed according to International Headache Society criteria and 111 matched controls were studied. Phenotype and allele frequencies were similarly distributed in patients and controls except for an iNOS (NOS2A) pentanucleotide repeat allele which was significantly more common in controls. We observed a higher phenotype frequency of this allele in our control group compared with rates in control groups of other studies, whereas the frequency in our patients was similar to that in controls from previous reports. Thus, we conclude that it is unlikely that genetic variations within the NOS genes contribute greatly to cluster headache susceptibility.

scholarly journals α-Adrenergic vasoreactivity of canine intrapulmonary bronchial arteries in pacing-induced heart failure

1999 ◽  
Vol 277 (4) ◽  
pp. H1392-H1402
Author(s):  
Ronald K. McMillon ◽  
Mary I. Townsley
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Control Group ◽  
Control Groups ◽  
Bronchial Arteries ◽  
Branching Order ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Dose Responses ◽  
Oxide Synthase

We hypothesized that pacing-induced congestive heart failure alters α-adrenergic constriction in intrapulmonary bronchial arteries. Cumulative dose responses to norepinephrine (NE), phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP) were determined in pressurized vessel segments. ED50values for NE and PE were higher for control (−5.34 ± 0.09 and −4.27 ± 0.08 M, respectively) vs. paced (−5.73 ± 0.10 and −5.06 ± 0.28 M, respectively) groups. Prazosin increased the ED50 values for NE and PE in both control and paced groups. Yohimbine decreased NE ED50 in the control group only. Endothelium removal or nitric oxide synthase (NOS) inhibition decreased control but not paced NE ED50. Maximum vasodilation and sensitivity (i.e., −ED50 values) were decreased for ACh but were similar for SNP in paced vs. control groups. Secondary segments were more reactive than paired primary segments in both groups, although pacing effects on ED50 were unrelated to branching order. In conclusion, adrenergic constriction of canine intrapulmonary bronchial arteries is predominantly mediated via α1-adrenoreceptors and is enhanced after pacing. Endothelium-derived relaxing factor(s) normally opposes α-adrenergic vasoconstriction but not after pacing in this vasculature.

CO2 laser enhances the chilling tolerance of wheat seedlings by stimulating NO synthesis

2016 ◽  
Vol 96 (5) ◽  
pp. 796-807
Author(s):  
Yi-ping Chen ◽  
Qiang Liu ◽  
Dong Chen
Keyword(s):  
Nitric Oxide ◽  
Laser Irradiation ◽  
Sodium Tungstate ◽  
Chilling Stress ◽  
Chilling Tolerance ◽  
The Other ◽  
Control Group ◽  
Wheat Seedlings ◽  
Oxide Synthase ◽  
Protein Treatment

To investigate the mechanism by which laser irradiation enhances the chilling tolerance of wheat seedlings, seeds were exposed to different treatments, and biochemical parameters were measured. Compared with the control group, chilling stress (CS) led to an increase in the concentrations of malondialdehyde (MDA) and H2O2, and decreases in the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), catalase (CAT), peroxidase (POD), and nitric oxide synthase (NOS), and the concentrations of nitric oxide (NO) and protein. Treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), sodium tungstate (ST), and NG-nitro-L-arginine methyl ester (L-NAME) followed by CS resulted in further increases in the concentrations of MDA and H2O2 and further decreases in the other parameters. However, treatment with PTIO, ST, and L-NAME followed by laser irradiation had the opposite effects on these parameters. When the seeds were treated with PTIO, ST, and L-NAME followed by laser and CS, the concentrations of MDA and H2O2 were significantly lower and the other parameters were higher than in the PTIO, ST, and L-NAME plus CS groups. These results suggest that CO2 laser irradiation enhances the chilling tolerance of wheat seedlings by stimulating endogenous NO synthesis.

Selective iNOS Inhibition Attenuates Acetylcholine- and Bradykinin-induced Vasoconstriction in Lipopolysaccharide-exposed Rat Lungs 

1999 ◽  
Vol 91 (6) ◽  
pp. 1724-1724 ◽  
Author(s):  
Lars G. Fischer ◽  
Damian J. Horstman ◽  
Klaus Hahnenkamp ◽  
Nancy E. Kechner ◽  
George F. Rich
Keyword(s):  
Nitric Oxide ◽  
Exhaled Nitric Oxide ◽  
Control Group ◽  
Biochemical Engineering ◽  
Inos Inhibitor ◽  
Nos Inhibitor ◽  
Inos Inhibitors ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Dose Dependent

Background Nonselective nitric oxide synthase (NOS) inhibition has detrimental effects in sepsis because of inhibition of the physiologically important endothelial NOS (eNOS). The authors hypothesized that selective inducible NOS (iNOS) inhibition would maintain eNOS vasodilation but prevent acetylcholine- and bradykinin-mediated vasoconstriction caused by lipopolysaccharide-induced endothelial dysfunction. Methods Rats were administered intraperitoneal lipopolysaccharide (15 mg/kg) with and without the selective iNOS inhibitors L-N6-(1-iminoethyl)-lysine (L-NIL, 3 mg/kg), dexamethasone (1 mg/kg), or the nonselective NOS inhibitor Nomega-nitro-L-arginine methylester (L-NAME, 5 mg/kg). Six hours later, the lungs were isolated and pulmonary vasoreactivity was assessed with hypoxic vasoconstrictions (3% O2), acetylcholine (1 microg), Biochemical Engineering, and bradykinin (3 microg). In additional lipopolysaccharide experiments, L-NIL (10 microM) or 4-Diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 100 microM), a selective muscarinic M3 antagonist, was added into the perfusate. Results Exhaled nitric oxide was higher in the lipopolysaccharide group (37.7+/-17.8 ppb) compared with the control group (0.4+/-0.7 ppb). L-NIL and dexamethasone decreased exhaled nitric oxide in lipopolysaccharide rats by 83 and 79%, respectively, whereas L-NAME had no effect. In control lungs, L-NAME significantly decreased acetylcholine- and bradykinin-induced vasodilation by 75% and increased hypoxic vasoconstrictions, whereas L-NIL and dexamethasone had no effect. In lipopolysaccharide lungs, acetylcholine and bradykinin both transiently increased the pulmonary artery pressure by 8.4+/-2.0 mmHg and 35.3+/-11.7 mmHg, respectively, immediately after vasodilation. L-NIL and dexamethasone both attenuated this vasoconstriction by 70%, whereas L-NAME did not. The acetylcholine vasoconstriction was dose-dependent (0.01-1.0 microg), unaffected by L-NIL added to the perfusate, and abolished by 4-DAMP. Conclusions In isolated perfused lungs, acetylcholine and bradykinin caused vasoconstriction in lipopolysaccharide-treated rats. This vasoconstriction was attenuated by administration of the iNOS inhibitor L-NIL but not with L-NAME. Furthermore, L-NIL administered with lipopolysaccharide preserved endothelium nitric oxide-dependent vasodilation, whereas L-NAME did not.

scholarly journals Analysis of NOS Gene Polymorphisms in Relation to Cluster Headache and Predisposing Factors in Sweden

2020 ◽  
Vol 11 (1) ◽  
pp. 34
Author(s):  
Caroline Ran ◽  
Julia M. Michalska ◽  
Carmen Fourier ◽  
Christina Sjöstrand ◽  
Elisabet Waldenlind ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cluster Headache ◽  
Genetic Variants ◽  
Potential Candidate ◽  
Nitric Oxide Signaling ◽  
Minor Alleles ◽  
Oxide Synthase ◽  
Trigeminal Reflex ◽  
Inducible Nos ◽  
Nos Gene

Cluster headache is characterized by activation of the autonomic-trigeminal reflex. Nitric oxide can trigger headaches in patients, and nitric oxide signaling is known to be affected in cluster headache. Based on the hypothesis of nitric oxide being involved in cluster headache pathophysiology we investigated nitric oxide synthases as potential candidate genes for cluster headache. We analyzed eight variants in the three forms of nitric oxide synthase (NOS) genes, inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS), and tested for association with cluster headache. Swedish cluster headache patients (n = 542) and controls (n = 581) were genotyped using TaqMan® assays on an Applied Biosystems 7500 qPCR cycler. This is the largest performed genetic study on NOS involvement in cluster headache so far. We found an association between cluster headache and one iNOS haplotype consisting of the minor alleles of rs2297518 and rs2779249 (p = 0.022). In addition, one of the analyzed nNOS variants, rs2682826, was associated with reported triptan use (p = 0.039). Our data suggest that genetic variants in NOS genes do not have a strong influence on cluster headache pathophysiology, but that certain combinations of genetic variants in NOS genes may influence the risk of developing the disorder or triptan use.

Developmental changes in nitric oxide synthase isoform expression and nitric oxide production in fetal baboon lung

2002 ◽  
Vol 283 (6) ◽  
pp. L1192-L1199 ◽  
Author(s):  
Philip W. Shaul ◽  
Sam Afshar ◽  
Linda L. Gibson ◽  
Todd S. Sherman ◽  
Jay D. Kerecman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Critical Role ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Developmental Changes ◽  
No Production ◽  
Third Trimester ◽  
Isoform Expression ◽  
Oxide Synthase ◽  
Nos Isoforms

Nitric oxide (NO), produced by NO synthase (NOS), plays a critical role in multiple processes in the lung during the perinatal period. To better understand the regulation of pulmonary NO production in the developing primate, we determined the cell specificity and developmental changes in NOS isoform expression and action in the lungs of third-trimester fetal baboons. Immunohistochemistry in lungs obtained at 175 days (d) of gestation (term = 185 d) revealed that all three NOS isoforms, neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), are primarily expressed in proximal airway epithelium. In proximal lung, there was a marked increase in total NOS enzymatic activity from 125 to 140 d gestation due to elevations in nNOS and eNOS, whereas iNOS expression and activity were minimal. Total NOS activity was constant from 140 to 175 d gestation, and during the latter stage (160–175 d gestation), a dramatic fall in nNOS and eNOS was replaced by a rise in iNOS. Studies done within 1 h of delivery at 125 or 140 d gestation revealed that the principal increase in NOS during the third trimester is associated with an elevation in exhaled NO levels, a decline in expiratory resistance, and greater pulmonary compliance. Thus, there are developmental increases in pulmonary NOS expression and NO production during the early third trimester in the primate that may enhance airway and parenchymal function in the immediate postnatal period.

Functional vagal input to chemically identified neurons in pancreatic ganglia as revealed by Fos expression

1999 ◽  
Vol 277 (5) ◽  
pp. E958-E964 ◽  
Author(s):  
Jiulin Wang ◽  
Huiyuan Zheng ◽  
Hans-Rudolf Berthoud
Keyword(s):  
Nitric Oxide ◽  
Vagal Stimulation ◽  
Significant Proportion ◽  
The Body ◽  
Identified Neurons ◽  
Stimulation Parameters ◽  
Unilateral Stimulation ◽  
Excitatory Synaptic Input ◽  
Fos Expression ◽  
Oxide Synthase

The importance of neural elements in the control of both endocrine and exocrine pancreatic secretory functions and their coordination with gastrointestinal, hepatic, and general homeostatic functions is increasingly recognized. To better characterize the vagal efferent input to the pancreas, the capacity of electrical vagal stimulation to induce expression of c-Fos in neurochemically identified neurons of intrapancreatic ganglia was investigated. At optimal stimulation parameters, unilateral stimulation of either the left or right cervical vagus induced Fos expression in ∼30% of neurons in the head and 10–20% of neurons in the body and tail of the pancreas. There was no Fos expression if no stimulation or stimulation with a distally cut vagus was applied. Large proportions of neurons contained nitric oxide synthase as assessed with NADPH diaphorase histochemistry (88%) and choline acetyltransferase. The proportion of nitrergic and nonnitrergic neurons receiving vagal input was not different. It is concluded that a significant proportion of pancreatic neurons receives excitatory synaptic input from vagal preganglionic axons and that many of these vagal postganglionic neurons can produce nitric oxide and acetylcholine.

scholarly journals SALMONELLA TYPHIMURIUM INFECTION: ANTIOXIDANT STATUS OF INFECTED POULTRY AND EFFICACY OF TREATMENT WITH KHAYA GRANDIFOLIOLA EXTRACT

2021 ◽  
Vol 10 (3) ◽  
pp. 72-79
Author(s):  
Elodie Yamako Konack ◽  
Jean Baptiste Sokoudjou ◽  
Norbert Kodjio ◽  
Gabriel Tchuente Kamsu ◽  
Huguette Bocanestine Laure Feudjio ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Biochemical Markers ◽  
Broiler Chickens ◽  
Antioxidant Status ◽  
Antioxidant Activities ◽  
The Body ◽  
Control Group ◽  
Enzymatic Antioxidants ◽  
Salmonella Infections

Salmonella infections remain one of the major health problems in both poultry farming and human medicine. In addition, resistance to Salmonella has emerged as a global health problem in both sectors. The present study aimed at evaluating the in vivo antisalmonellal and antioxidant activities of 95° ethanol extract of Khaya grandifoliola using broiler chickens as animal model. Animals were divided into the normal control group, negative control group, positive control group and three test groups treated with the extract at 10, 20 and 40 mg/kg respectively. The antioxidant status of broiler chickens was also evaluated by measuring the concentration of enzymatic antioxidants (catalase, glutathione peroxidase) and biochemical markers (malondialdehyde and nitric oxide). The results showed that infected animals treated with the Khaya grandifoliola extract at 40 mg/kg recovered on day 11 after the beginning of the treatment and on day 13 for those treated at the 10 and 20 mg/kg. The antioxidant assay showed that the infection led to the reduction of enzymatic markers in the body of infected animals, while the treatment increases such makers. The infection resulted in a significant increase in serum and pulmonary malondialdehyde. It also caused a significant decrease in cardiac and pulmonary nitric oxide whereas the treatment depending on the doses of the extract tends to normalize these biochemical markers. The overall results showed that Khaya grandifoliola extract can be successfully used in the treatment of avian salmonellosis as well as the management of the oxidative stress caused by the infection.

scholarly journals Preventive Effect of Lactobacillus Plantarum CQPC10 on Activated Carbon Induced Constipation in Institute of Cancer Research (ICR) Mice

2018 ◽  
Vol 8 (9) ◽  
pp. 1498 ◽  
Author(s):  
Jing Zhang ◽  
Xianrong Zhou ◽  
Benshou Chen ◽  
Xingyao Long ◽  
Jianfei Mu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Activated Carbon ◽  
Nitric Oxide Synthase ◽  
Lactobacillus Plantarum ◽  
Quantitative Polymerase Chain Reaction ◽  
Inhibitory Effect ◽  
Lactobacillus Bulgaricus ◽  
Control Group ◽  
Expression Levels ◽  
Oxide Synthase

Chinese Paocai is a traditional fermented food containing an abundance of beneficial microorganisms. In this study, the microorganisms in Szechwan Paocai were isolated and identified, and a strain of lactic acid bacteria (Lactobacillus plantarum CQPC10, LP-CQPC10) was found to exert an inhibitory effect on constipation. Microorganisms were isolated and identified via 16S rDNA. Activated carbon was used to induce constipation in a mouse model and the inhibitory effect of LP-CQPC10 on this induced constipation was investigated via both pathological sections and qPCR (quantitative polymerase chain reaction). A strain of Lactobacillus plantarum was identified and named LP-CQPC10. The obtained results showed that, as compared to the control group, LP-CQPC10 significantly inhibited the amount, weight, and water content of faeces. The defecation time of the first tarry stool was significantly shorter in LP-CQPC10 groups than in the control group. The activated carbon progradation rate was significantly higher when compared to the control group and the effectiveness was improved. LP-CQPC10 increased the serum levels of MTL (motilin), Gas (gastrin), ET (endothelin), AchE (acetylcholinesterase), SP (substance P), and VIP (vasoactive intestinal peptide), while decreasing the SS (somatostatin) level. Furthermore, it improved the GSH (glutathione) level and decreased the MPO (myeloperoxidase), MDA (malondialdehyde), and NO (nitric oxide) levels. The results of qPCR indicated that LP-CQPC10 significantly up-regulated the mRNA expression levels of c-Kit, SCF (stem cell factor), GDNF (glial cell-derived neurotrophic factor), eNOS (endothelial nitric oxide synthase), nNOS (neuronal nitric oxide synthase), and AQP3 (aquaporin-3), while down-regulating the expression levels of TRPV1 (transient receptor potential cation channel subfamily V member 1), iNOS (inducible nitric oxide synthase), and AQP9 (aquaporin-9). LP-CQPC10 showed a good inhibitory effect on experimentally induced constipation, and the obtained effectiveness is superior to that of Lactobacillus bulgaricus, indicating the better probiotic potential of this strain.

Impaired nitric oxide-mediated vasodilation in transgenic sickle mouse

2000 ◽  
Vol 278 (6) ◽  
pp. H1799-H1806 ◽  
Author(s):  
Dhananjaya K. Kaul ◽  
Xiao-Du Liu ◽  
Mary E. Fabry ◽  
Ronald L. Nagel
Keyword(s):  
Nitric Oxide ◽  
Transgenic Mice ◽  
Endothelial Nitric Oxide Synthase ◽  
Vascular Tone ◽  
Endothelial Damage ◽  
Control Groups ◽  
Lower Blood ◽  
Activating Agent ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Transgenic sickle mice expressing human βS- and βS-Antilles-globins show intravascular sickling, red blood cell adhesion, and attenuated arteriolar constriction in response to oxygen. We hypothesize that these abnormalities and the likely endothelial damage, also reported in sickle cell anemia, alter nitric oxide (NO)-mediated microvascular responses and hemodynamics in this mouse model. Transgenic mice showed a lower mean arterial pressure (MAP) compared with control groups (90 ± 7 vs. 113 ± 8 mmHg, P < 0.00001), accompanied by increased endothelial nitric oxide synthase (eNOS) expression. NG-nitro-l-arginine methyl ester (l-NAME), a nonselective inhibitor of NOS, caused an ∼30% increase in MAP and ∼40% decrease in the diameters of cremaster muscle arterioles (branching orders: A2 and A3) in both control and transgenic mice, confirming NOS activity; these changes were reversible after l-arginine administration. Aminoguanidine, an inhibitor of inducible NOS, had no effect. Transgenic mice showed a decreased ( P < 0.02–0.01) arteriolar dilation in response to NO-mediated vasodilators, i.e., ACh and sodium nitroprusside (SNP). Indomethacin did not alter the responses to ACh and SNP. Forskolin, a cAMP-activating agent, caused a comparable dilation of A2 and A3 vessels (∼44 and 70%) in both groups of mice. Thus in transgenic mice, an increased eNOS/NO activity results in lower blood pressure and diminished arteriolar responses to NO-mediated vasodilators. Although the increased NOS/NO activity may compensate for flow abnormalities, it may also cause pathophysiological alterations in vascular tone.

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