Pulmonary vascular dilation induced by l‐arginine: correlation with induction of endothelial nitric oxide synthase in a rabbit model

2005 ◽  
Vol 46 (1) ◽  
pp. 48-54 ◽  
Author(s):  
S. K. Yoon ◽  
K.‐N. Lee ◽  
J. H. Lee ◽  
J. S. Jeong ◽  
J.‐Y. Kwak
Keyword(s):  
Nitric Oxide ◽  
Computed Tomography ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Tap Water ◽  
Rabbit Model ◽  
Serum Levels ◽  
Control Group ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Purpose: To determine whether oral administration of l‐arginine induces pulmonary vascular dilation, and if this pulmonary vascular dilation correlates with induction of endothelial nitric oxide synthase (eNOS) in a rabbit model. Material and Methods: Seven rabbits were fed with l‐arginine dissolved in tap water. The degree of pulmonary vascular dilation was determined using thin‐section computed tomography and the concentration of serum nitrite was measured. They were compared with four control animals. The pulmonary vascular dilation was correlated to serum levels of nitrite. Lung tissues were examined for induction of eNOS by immunohistochemistry. Results: An increased degree of pulmonary vascular dilation was found in the l‐arginine‐fed group compared to the control group ( P<0.05). Serum levels of nitrite in the l‐arginine‐fed group were higher than those in the control group ( P<0.05). Pulmonary vascular dilation correlated with serum levels of nitrite ( r2 = 0.95, P<0.05). Induction of eNOS was increased in the l‐arginine‐fed group. Conclusion: The administration of l‐arginine causes pulmonary vascular dilation, which is most likely mediated via nitric oxide through increased induction of eNOS in a rabbit model.

Using endothelial nitric oxide synthase gene polymorphisms to identify intracranial aneurysms more prone to rupture in Japanese patients

2006 ◽  
Vol 105 (5) ◽  
pp. 717-722 ◽  
Author(s):  
Boris Krischek ◽  
Hidetoshi Kasuya ◽  
Hiroyuki Akagawa ◽  
Atsushi Tajima ◽  
Akira Narita ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Intracranial Aneurysms ◽  
Tandem Repeats ◽  
Japanese Patients ◽  
Control Group ◽  
Patient Sample ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Object Recent investigators found that the presence of three tandem polymorphisms of the endothelial nitric oxide synthase (eNOS) gene—promoter single nucleotide polymorphism (SNP) T-786C, intron-4 27-bp variable number of tandem repeats, and the G894T SNP in exon 7—was indicative of intracranial aneurysms more prone to rupture in a Caucasian patient sample. In the present study, the authors sought to determine whether the presence of these eNOS polymorphisms could indicate which Japanese patients with aneurysms were more endangered by a subarachnoid hemorrhage (SAH). Methods The three eNOSpolymorphisms were genotyped in 297 patients with ruptured aneurysms (RAs), 108 patients with unruptured aneurysms (UAs), and 176 healthy volunteers by using polymerase chain reaction. The distribution of the variant alleles did not differ significantly (p > 0.05) between the RA group and the UA group. The frequency of the corresponding genotypes between the two groups and a haplotype analysis did not show any significant differences. Further comparisons of the RA and UA groups with the control group did not yield any significant allele or genotype frequency differences. Conclusions These data show that the examined set of eNOS polymorphisms were not indicative of which Japanese patients with intracranial aneurysms would suffer an SAH. The presence of eNOS polymorphisms is not useful in identifying intracranial aneurysms that are more prone to rupture in a Japanese patient sample.

Prevalence of common polymorphisms of AT-rich interaction domain 1A and endothelial nitric oxide synthase in patients with endometriosis compared to control group

2018 ◽  
Vol 10 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Zohreh Tavana ◽  
Azadeh Khalili ◽  
Golnaz Namazi ◽  
Ahmad Ebrahimi ◽  
Sara Davoodi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Control Group ◽  
Enos Gene ◽  
Interaction Domain ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Rich Interaction ◽  
Glu298asp Polymorphism

Introduction: Endometriosis is a common gynecologic disorder defined as ectopic presence of endometrial tissue in extrauterine sites. Endometriosis is associated with infertility and risk of malignancy. Identification of genetic factors responsible for development and malignant transformation of endometriosis can improve therapeutic approaches. In this study, we investigated the association of AT-rich interaction domain 1A ( ARID1A) and endothelial nitric oxide synthase ( eNOS) polymorphisms with endometriosis and staging of the disease. Methods: A total of 100 women with laparoscopy-confirmed diagnosis of endometriosis were included and compared with 100 women without endometriosis as the control group. Genotypes of patients regarding Gln920Ter polymorphism of ARID1A gene and Glu298Asp polymorphism of eNOS gene were determined by polymerase chain reaction techniques on blood samples from the study population. The prevalence of each genotype in endometriosis patients was compared with healthy controls using the chi-square test. Results: Significantly higher prevalence of non-CC genotype for ARID1A Gln920Ter polymorphism and non-GG genotype for G894T polymorphism of the eNOS gene was detected in the endometriosis group. There was no significant relationship between these polymorphisms and staging of endometriosis. Discussion: Significant variation of prevalence of Gln920Ter polymorphism of the ARID1A gene and Glu298Asp polymorphism of the eNOS gene among the two groups can indicate a causative effect of these genetic alterations on the development of endometriosis.

scholarly journals Synthetic Pyridoindole and Rutin Affect Upregulation of Endothelial Nitric Oxide Synthase and Heart Function in Rats Fed a High-Fat-Fructose Diet

2021 ◽  
pp. 851-863
Author(s):  
L. Salvaras ◽  
T. Kovacic ◽  
P. Janega ◽  
B. Liptak ◽  
M. Sasvariova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Left Ventricle ◽  
Endothelial Nitric Oxide Synthase ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Control Group ◽  
High Fat ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Metabolic syndrome (MetS) belongs to the serious health complications expanding in cardiovascular diseases, obesity, insulin resistance, and hyperglycemia. In this study, hypertriacylglycerolemic rats fed a high-fat-fructose diet (HFFD) were used as an experimental model of MetS to explore the effect of tested compounds. Effects of a new prospective pyridoindole derivative coded SMe1EC2 and the natural polyphenol rutin were tested. Endothelial nitric oxide synthase (NOS3) and nuclear factor kappa B (NF-κB) expression were assessed in the left ventricle immunohistochemically and left ventricle activity was monitored in isolated perfused rat hearts. NOS3 activity in the left ventricle decreased markedly as a result of a HFFD. NOS3 expression was upregulated by both substances. NF-κB expression was increased in the MetS group in comparison to control rats and the expression further increased in the SMe1EC2 treatment. This compound significantly improved the coronary flow in comparison to the control group during reperfusion of the heart followed after ischemia. Further, it tended to increase left ventricular systolic pressure, heart product, rate of maximal contraction and relaxation, and coronary flow during baseline assessment. Moreover, the compound SMe1EC2 decreased the sensitivity of hearts to electrically induced ventricular fibrillation. Contrary to this rutin decreased coronary flow in reperfusion. Present results suggest that despite upregulation of NOS3 by both substances tested, pyridoindole SMe1EC2 rather than rutin could be suitable in treatment strategies of cardiovascular disorders in MetS-like conditions.

scholarly journals Muscle contraction induced arterial shear stress increases endothelial nitric oxide synthase phosphorylation in humans

2017 ◽  
Vol 313 (4) ◽  
pp. H854-H859 ◽  
Author(s):  
Darren P. Casey ◽  
Kenichi Ueda ◽  
Lauren Wegman-Points ◽  
Gary L. Pierce
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Synthase ◽  
Brachial Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Control Group ◽  
Time Control ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Male Subjects

We determined if local increases in brachial artery shear during repetitive muscle contractions induce changes in protein expression of endothelial nitric oxide synthase (eNOS) and/or phosphorylated (p-)eNOS at Ser1177, the primary activation site on eNOS, in endothelial cells (ECs) of humans. Seven young male subjects (25 ± 1 yr) performed 20 separate bouts (3 min each) of rhythmic forearm exercise at 20% of maximum over a 2-h period. Each bout of exercise was separated by 3 min of rest. An additional six male subjects (24 ± 1 yr) served as time controls (no exercise). ECs were freshly isolated from the brachial artery using sterile J-wires through an arterial catheter at baseline and again after the 2-h exercise or time control period. Expression of eNOS or p-eNOS Ser1177 in ECs was determined via immunofluorescence. Brachial artery mean shear rate was elevated compared with baseline and the time control group throughout the 2-h exercise protocol ( P < 0.001). p-eNOS Ser1177 expression was increased 57% in ECs in the exercise group [0.06 ± 0.01 vs. 0.10 ± 0.02 arbitrary units (au), P = 0.02] but not in the time control group (0.08 ± 0.01 vs. 0.07 ± 0.01 au, P = 0.72). In contrast, total eNOS expression did not change in either the exercise (0.13 ± 0.04 vs. 0.12 ± 0.03 au) or time control (0.12 ± 0.03 vs. 0.11 ± 0.03 au) group ( P > 0.05 for both). Our novel results suggest that elevations in brachial artery shear increase eNOS Ser1177 phosphorylation in the absence of changes in total eNOS in ECs of young healthy male subjects, suggesting that this model is sufficient to alter posttranslational modification of eNOS activity in vivo in humans. NEW & NOTEWORTHY Elevations in brachial artery shear in response to forearm exercise increased endothelial nitric oxide synthase Ser1177 phosphorylation in brachial artery endothelial cells of healthy humans. Our present study provides the first evidence in humans that muscle contraction-induced increases in conduit arterial shear lead to in vivo posttranslational modification of endothelial nitric oxide synthase activity in endothelial cells.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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