eNOS Gene Polymorphisms Research Articles

Associations between endothelial nitric oxide synthase A/B, angiotensin converting enzyme I/D and serotonin transporter L/S gene polymorphisms with pulmonary hypertension in COPD patients

Different biochemical pathways and cellular mechanisms play role in the pathogenesis of pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD). Alveolar hypoxia is not the only determinant of vascular remodeling, genetic factors are thought to have additive effects. We aimed to investigate the effects of endothelial nitric oxide synthase (eNOS A/B), angiotensin converting enzyme (ACE I/D) and serotonin transporter (5-HTT L/S) gene polymorphisms on development and severity of PH in COPD patients. 50 COPD patients without PH (group 1); 30 COPD patients with PH confirmed with echocardiography (group 2) and 49 healthy subjects (group 3) as control group were included to the study. eNOS A/B, ACE I/D and 5-HTT L/S gene polymorphisms and allele frequencies of COPD patients with and without PH and healthy subjects were determined. Functional parameters and echocardiographic measurements were recorded. Patients with PH were also assessed in two subgroups according to the severity of pulmonary arterial pressure (PAP). Significant differences among three groups in the distribution of 5-HTT genotype and allele frequency were present (respectively p = 0.002; p = 0.021). In group 2, LL and LS genotype rate was 93.3 % with a frequency of 71.2 % L allele and 28.3 % of S allele. 5-HTT LL genotype was present in 88.9 % of patients with PAP ≥50 mmHg significantly (p = 0.012). Other genotype distributions were not significantly different between two subgroups. The results of this study can suggest that COPD patients with L allele of 5-HTT may have higher risk for the development of PH and patients with LL genotype of 5-HTT may present higher PAP. We also demonstrated that eNOS and ACE gene polymorphisms were not associated with the development and severity of PH in our study population. Further studies with larger numbers of patients are needed to explore these relationships.

The −974C>A (rs3087459) gene polymorphism in the endothelin gene (EDN1) is associated with risk of developing acute coronary syndrome in Mexican patients

Endothelial dysfunction plays an essential role in the development and progression of atherosclerotic lesions. Endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) are considered important molecules in the endothelial dysfunction process. The aim of the present study was to evaluate the role of eNOS and ET-1 (EDN1) gene polymorphisms as susceptibility markers for acute coronary syndrome (ACS). Six polymorphisms (rs1799983, rs2070744, rs1800783, rs3087459, rs1800541, and rs5369) of eNOS and EDN1 genes were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 452 patients with ACS and 283 healthy controls. The results showed increased frequencies of the A allele of the END1-914 C>A (rs3087459) polymorphism in ACS patients when compared to controls (OR=1.56, Pc=0.01). Under an additive model, the "AA" genotype was associated with an increased risk of developing ACS, adjusted for gender, hypertension, dyslipidemia, alcohol consumption, smoking, and diabetes (OR=1.56, p=0.045). Linkage disequilibrium analysis showed one EDN1 haplotype (AT) with increased frequency in ACS patients when compared to healthy controls (OR=1.65, Pc=0.0015). The "AT" haplotype was associated with the risk of developing ACS after adjusting for cardiovascular risk factors using multiple logistic analysis. In this case, the adjusted OR was 1.73 for the AT haplotype (Pc=0.0018). In summary, resulting data suggest that the END1-914 C>A gene polymorphism could be involved in the risk of developing ACS in Mexican individuals.

Endothelial nitric oxide synthase (eNOS) (Glu298Asp) and urotensin II (UTS2 S89N) gene polymorphisms in preeclampsia: prediction and correlation with severity in Egyptian females

Background: Preeclampsia is a leading cause of maternal and fetal/neonatal morbidity and mortality. Early prediction of preeclampsia can minimize maternal and fetal complications. Gene polymorphisms are promising markers for early prediction of preeclampsia. Aim of work: To assess the value of endothelial nitric oxide synthase (eNOS) (Glu298Asp) and urotensin II (UTS2 S89N) gene polymorphisms for early prediction of preeclampsia. Methods: The preeclamptic group consisted of 53 pregnant who developed preeclampsia (35 mild and 18 severe), while the control group consisted of 65 age-matched pregnant females who completed uncomplicated pregnancies. eNOS and urotensin II gene polymorphisms were tested using polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP). Results: Concerning the eNOS gene polymorphism, there were highly significant differences between the two groups regarding the GG genotype as well as the G and T allele frequency (p < 0.001) and a statistically significant differences regarding the GT, TT genotypes (p = 0.002, 0.0276, respectively). Concerning the urotensin II gene polymorphisms, there were highly significant differences regarding the SS, SN genotypes as well as the S and N allele frequency (p < 0.001), statistically significant differences regarding the NN genotype (p = 0.063). Conclusion: Women having mutation in any of the two studied genes are at risk to develop mild preeclampsia, and those having mutations in both genes are at risk to develop severe preeclampsia, while the females with normal pregnancy are protected by the higher percentage of expression of the normal (wild allelles) of both genes.

ENDOTHELIAL NITRIC OXIDE SYNTHASE (ENOS) GENE POLYMORPHISM IS ASSOCIATED WITH AGE ONSET OF MENARCHE IN SICKLE CELL DISEASE FEMALES OF INDIA

Background and ObjectiveFemales with sickle cell disease (SCD) often show late onset of menarche. In transgenic sickle cell mouse, deficiency of gene encoding endothelial nitric oxide synthase (eNOS) has been reported to be associated with late onset of menarche. Thus to explore the possible association of eNOS gene polymorphism with age of onset of menarche in SCD females, 3 important eNOS gene polymorphisms- eNOS 4a/b, eNOS 894G>T (rs1799983) and eNOS-786 T>C (rs2070744) and plasma nitrite levels were tested among three groups of females- SCD late menarche, SCD early menarche and control females.MethodologyAbout 39 SCD females comprising of 18 SCD early menarche and 21 SCD late menarche groups were studied along with 48 control females. Genotyping of eNOS gene polymorphisms were done by PCR-RFLP and quantification of plasma nitrite level was performed by ELISA based commercial kits.ResultsSCD late menarche females showed significantly higher prevalence and higher association of heterozygous genotypes, higher frequency of mutant alleles .4a., .T. and .C. as compared to that of control group and SCD early menarche group. The frequency of haplotype .4a-G-C. and haplotype .4b-G-C. (alleles in order of eNOS 4a/b, eNOS 894G>T and eNOS-786 T>C respectively) were found to be significantly high in SCD late menarche compared to combined groups of SCD early menarche and controls. SCD late menarche group had significantly low level of plasma nitrite concentration for all 3 eNOS gene polymorphisms as compared to controls and SCD early menarche females.ConclusioneNOS gene polymorphism may influence age of onset of menarche in SCD females.

AB0235 Genetic polymorphisms of endothelial nitric oxide synthase (ENOS) and dermic expression of ENOS/INOS in mexican patients with systemic sclerosis. A preliminary report

BackgroundVascular dysfunction usually preceds clinically detectable fibrosis of systemic sclerosis (SSc). Vascular affection occurs more frequently in limited subtype of SSc (lcSSc) than diffuse subtype (dcSSc). The eNOS catalyses the...

AB0504 Vascular differences associated to genetic polymorphisms of endothelial nitric oxide synthase in mexican patients with systemic sclerosis.

BackgroundVascular dysfunction usually is observed before clinically detectable fibrosis of systemic sclerosis (SSc). The eNOS catalyses the synthesis of nitric oxide (NO), which maintains basal vascular tone and endothelial function....

Endothelial nitric oxide synthase gene intron 4 polymorphism in non-traumatic osteonecrosis of the femoral head

PurposeNitric oxide (NO) synthesised by endothelial NO synthase (eNOS) is a potent regulator of internal haemodynamics. A polymorphism in intron 4 of the eNOS is associated with different vascular disorders. We investigated the potential involvement of this polymorphism in idiopathic and secondary osteonecrosis of the femoral head (ONFH) in Polish patients.MethodsWe performed a study involving 68 patients with ONFH (45 idiopathic and 23 secondary) and 100 healthy controls. All subjects were genotyped for the eNOS4 polymorphism by the polymerase chain reaction followed by agarose gel electrophoresis.ResultsThe analysis revealed that the frequencies of eNOS4 genotypes were significantly different in ONFH patients (both idiopathic and secondary) than in controls. The frequencies of the 4a allele were significantly higher in the total group of patients versus controls [22.79 vs 9 %, p = 0.00039, odds ratio (OR) 2.98]. In subgroup analysis the 4a allele increased significantly in both idiopathic (20 vs 9 %, p = 0.0074, OR = 2.52) and secondary (28.26 vs 9 %, p = 0.00047, OR = 3.98) ONFH patients compared to control subjects. The frequency of the 4a/b genotype in the total group of patients (36.76 vs 16 %, p = 0.0011, OR = 3.24) as well as patients with idiopathic (35.56 vs 16 %, p = 0.0069, OR = 2.96) and secondary (39.13 vs 16 %, p = 0.0073, OR = 3.89) ONFH was higher than in the control group.ConclusionsThere was a significantly higher frequency of eNOS 4a allele carriers among the total group of patients as well as in idiopathic and secondary ONFH. This suggests that the eNOS gene polymorphism may be associated with increased risk of ONFH.

Relationship between endothelial nitric oxide synthase gene polymorphisms and ischemic stroke: a meta-analysis

Previous studies examining whether polymorphisms (G894T, 4b/a, and T786C) in the endothelial nitric oxide synthase (eNOS) gene are associated with ischemic stroke have yielded conflicting results. We performed a meta-analysis to investigate the potential association between these three eNOS gene polymorphisms and ischemic stroke risk. We searched databases until April 30, 2012 and used fixed or random effects models to estimate the pooled odds ratios (ORs). We analyzed 34 case-control data sets from 33 publications involving 5261/5823 cases/controls for G894T, 4295/4682 for 4b/a, and 2698/3254 for T786C polymorphisms. For Asian populations, all models showed significantly increased risk of ischemic stroke for the G894T (dominant model: OR = 1.58; 95% CI, 1.30-1.91; P = 0.000) and 4b/a polymorphisms (dominant model: OR = 1.46; 95% CI, 1.25-1.71; P = 0.000), even after Bonferroni correction (because 0.000 < 0.017). In white populations, the aa genotype seemed to be protective for ischemic stroke, as indicated by the recessive model (OR = 0.44; 95% CI, 0.22-0.87; P = 0.019). In Asian populations, the T786C polymorphism was significantly associated with ischemic stroke, as found using the dominant (OR = 1.17; 95% CI, 1.02-1.34; P = 0.025) and additive models (OR = 1.18; 95% CI, 1.05-1.33; P = 0.006). Our comprehensive meta-analysis ascertains that the G894T, 4b/a, and T786C polymorphisms are associated with ischemic stroke risk in Asians. A possible contrasting role of the 4b/a polymorphism in ischemic stroke was indicated in white populations.

Association of eNOS (E298D) and CYP2J2 (−50 G/T) gene polymorphisms with hypertension among Egyptian cases

BackgroundHypertension is a multifactorial and polygenic disorder where several susceptible genes interact with the environmental factors. ObjectiveThis study was designed to investigate the frequency of the endothelial nitric oxide synthase (eNOS, E298D) and cytochrome P450 2J2 (CYP 2J2 −50G/T) gene polymorphisms among Egyptian hypertensive subjects. Subjects and methodsGenomic DNA was isolated from peripheral blood samples collected from 123 hypertensive cases and from 429 healthy non-related controls by using Magna pure system (Roche Molecular Biochemicals, Mannheim, Germany). DNA was used to determine the frequency of eNOS, E298D and CYP 2J2 −50G/T allelic variants using the Light Cycler polymerase chain reaction (Realtime PCR) technique. Genotype (wild type, mutant and heterozygous) was determined by melting curve analysis. ResultsRegarding the study of eNOS and CYP2J2 gene polymorphisms, analysis of total hypertensive cases exhibited higher frequency of mutant eNOS heterozygous ED genotype compared to controls, yet statistically insignificant (27.6% vs. 21.1%, OR=1.5, 95% CI=0.9–2.8, p=0.1). Similarly, analysis of hypertensive cases also exhibited higher frequency of mutant CYP2J2 −50GT genotypes compared to controls that was also statistically insignificant (13.8% vs. 10.7%, OR=1.3, 95% CI=0.7–2.4, p=0.4). All subgroups of hypertensive complicated cases either with cardiac diseases, with diabetic or with renal disorders showed insignificant difference compared to controls. ConclusionThe present study demonstrated no association between eNOS E298D and CYP2J2 −50 G/T gene polymorphisms and hypertension among Egyptian subjects.

Variants in endothelial nitric oxide synthase (eNOS) gene in idiopathic infertile Brazilian men

PurposeIn recent years, considerable concern has been expressed about the deleterious effects of reactive oxygen species (ROS) on sperm function, because ROS at high levels is potentially detrimental to sperm function and quality. Nitric oxide (NO) is a powerful anti-oxidant present in seminal plasma. The aim of the study was to analyze the distribution of the of endothelial nitric oxide synthase (eNOS) gene (T-786C, G894T, e 4a/b) polymorphisms in idiopathic infertile Brazilian men and evaluate the possible role of these polymorphisms in sperm count. MethodsA case–control study was performed comprising 208 infertile men [n=74 with non-obstructive azoospermia and n=134 with severe oligozoospermia] and 201 fertile men as controls. Genotyping of eNOS polymorphisms was performed by real time (T-786C and G894T) and conventional PCR (4a/b). The results were analyzed statistically and a p-value<0.05 was considered significant. ResultsAccording to the sperm count, relatively similar eNOS polymorphism genotypes and allele frequencies were found among the groups. Combined genotypes of the eNOS polymorphisms did not identify a haplotype associated with idiopathic infertility, even when the patients were separated in non-obstructive azoospermia or severe oligozoospermia. ConclusionIn conclusion, the findings demonstrate that, in Brazilian population studied, genetic variations, T-786C, G894T, and e 4a/b, of the eNOS gene are not associated with male infertility.

The relationship between coronary artery ectasia and eNOS intron 4a/b gene polymorphisms

Background Little is known about the pathogenesis and genetics of coronary artery ectasia (CAE). We studied eNOS gene intron 4a/b polymorphism in this patient population.Methods The study group included 30 patients with non-obstructive CAD besides CAE on coronary angiogram performed due to positive non-invasive diagnostic test results. The control group included 20 patients with normal coronary arteries. Agarose gel electrophoresis was used to identify eNOS gene polymorphisms.Results Only one coronary vessel was involved in most of the study cohort and the left anterior descending artery (LAD) was the most frequently involved vessel. The frequencies of eNOS gene phenotypes in the CAE group were 3.3% for “aa”, 53.3% for “ab” and they were higher than in the control group. However, statistical signifi cance was not reached (χ2 = 5.10, P= 0.08). When compared with the control group the presence of “a” type allele of eNOS gene was signifi cantly more frequent in the CAE group (χ2 = 4.88, P= 0.027). By univariate analysis, eNOS gene polymorphism was correlated with CAE but this signifi cance was attenuated after additional adjustment for potential confounding.Conclusion Patients who have the “a” type allele of the eNOS gene may have an increased risk for CAE.

Endothelial NOS gene Glu298Asp polymorphism in preterm neonates with respiratory distress syndrome

Respiratory Distress Syndrome (RDS) due to prematurity is one of the most important causes of morbidity and mortality in Neonatal Intensive Care Units. According to few studies in recent years, endothelial nitric oxide synthase (eNOS) gene polymorphisms are found to be partially responsible for liability to RDS. The purpose of this study was to determine the association between eNOS gene polymorphism and RDS in preterm neonates. The patient group consisted of 152 premature neonates born before 37 weeks of gestation and diagnosed as RDS. The control group consisted of 125 premature neonates born before 37 weeks of gestation, but was not diagnosed as RDS. Genomic DNA from patients and controls was analyzed by polymerase chain reaction. It was found that Glu/Glu, Glu/Asp, and Asp/Asp genotype frequencies of the eNOS gene polymorphism were 35.2%, 59.2%, and 5.6% of the control group, and 32.9%, 65.1%, and 2.0% of the patient group, respectively (P > 0.05). However, significant increases in Glu/Glu genotype and Glu allele frequencies were noted in the RDS groups when the preterm neonates were divided into two groups (24-30 weeks and 31-36 weeks) by gestational age. Additionally, Glu/Asp genotype and Asp allele were markedly less frequent among the RDS groups (P < 0.05). Asp allele frequency in boys and Glu allele frequency in girls were significantly high in RDS group (P < 0.05). These data suggest that there were significant gestational age-related differences between RDS and control groups in terms of Glu298Asp polymorphism. Therefore, RDS seems to develop with alterations in eNOS Glu298Asp genotype frequencies in the Turkish population.

Endothelial Nitric Oxide Synthase Gene Polymorphisms and Risk of Preeclampsia

Polymorphisms in endothelial nitric oxide synthase (eNOS) gene may affect the risk of preeclampsia. This systematic review aimed to provide an updated review of the literature to better understand the association between the eNOS gene polymorphisms and the risk of preeclampsia. We searched electronic databases of the human literature in PubMed, EMBASE, and the Cochrane Library up to July 2012. A meta-analysis was conducted on the association of eNOS G894T, T786C, and intron 4b/a polymorphisms with preeclampsia using (1) allele contrast, (2) recessive, (3) dominant, and (4) additive models. Thirty-three studies comprising 10,671 participants met the inclusion criteria. There was statistically significant association between the G894T variant and increased risk of preeclampsia (TT versus TG + GG: odds ratio 1.43, 95% confidence interval: 1.13 to 1.82). However, no significant risk of preeclampsia was observed either in the T786C or the intron 4b/a polymorphism. Homozygosity TT in eNOS G894T variant is significantly associated with an increased risk of preeclampsia.

ENOS gene variants and the risk of premature myocardial infarction.

BACKGROUND: Endothelial nitric oxide synthase (eNOS) as well as nitric oxide play an important role in the regulation of cardiovascular function. There are limited and controversial data regarding the impact of polymorphisms of eNOS gene that is implicated in the vasoconstrictive properties of the endothelium in the pathogenesis of premature myocardial infarction (MI).OBJECTIVE: We examined whether two common polymorphisms of eNOS gene (G894T and T786C) are associated with the development of premature MI.METHODS: We recruited 107 patients with premature MI and compared them to 103 age- and sex- matched controls. All patients underwent coronary angiogram and were classified into the subgroup of patients with ‘normal’ or ‘near normal’ coronary arteries and the subgroup of patients with significant coronary artery disease (≥ 50% stenosis in lumen diameter of coronary arteries). The genetic polymorphisms of eNOS gene were assayed with polymerase chain reaction and reverse hybridization.RESULTS: Nineteen patients (17.8%) had ‘normal’ or ‘near normal’ coronary arteries. A significantly higher frequency of homozygosity for the 786C (32%) and the 894T (21%) alleles of the eNOS gene in patients who develop early MI in the setting of angiographically 'normal' or 'near normal' coronary arteries were found.CONCLUSIONS: Our data suggest that the T786C and the G894T genetic polymorphisms are associated with the development of MI in very young individuals, whose coronary arteries are characterized by very small atheromatic burden.

ENOS Gene Variants and the Risk of Premature Myocardial Infarction

BACKGROUND: Endothelial nitric oxide synthase (eNOS) as well as nitric oxide play an important role in the regulation of cardiovascular function. There are limited and controversial data regarding the impact of polymorphisms of eNOS gene that is implicated in the vasoconstrictive properties of the endothelium in the pathogenesis of premature myocardial infarction (MI).OBJECTIVE: We examined whether two common polymorphisms of eNOS gene (G894T and T786C) are associated with the development of premature MI.METHODS: We recruited 107 patients with premature MI and compared them to 103 age- and sex- matched controls. All patients underwent coronary angiogram and were classified into the subgroup of patients with ‘normal’ or ‘near normal’ coronary arteries and the subgroup of patients with significant coronary artery disease (≥ 50% stenosis in lumen diameter of coronary arteries). The genetic polymorphisms of eNOS gene were assayed with polymerase chain reaction and reverse hybridization.RESULTS: Nineteen patients (17.8%) had ‘normal’ or ‘near normal’ coronary arteries. A significantly higher frequency of homozygosity for the 786C (32%) and the 894T (21%) alleles of the eNOS gene in patients who develop early MI in the setting of angiographically 'normal' or 'near normal' coronary arteries were found.CONCLUSIONS: Our data suggest that the T786C and the G894T genetic polymorphisms are associated with the development of MI in very young individuals, whose coronary arteries are characterized by very small atheromatic burden.

Association between VEGF and eNOS gene polymorphisms and lumbar disc degeneration in a young Korean population

Disturbances in blood flow to intervertebral discs (IVD) play an important role in IVD degeneration. Vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) are extremely important angiogenic factors for vasodilation and neovascularization. We investigated the relationship between single nucleotide polymorphisms (SNPs) of the VEGF and eNOS genes and genetic susceptibility to lumbar IVD degeneration in a young adult Korean population. Two hundred and forty-one participants (aged 18 to 30 years), with or without low back pain, were selected for the study. Magnetic resonance imaging was made of the lumbar spine in all participants. The patient group (N = 102) had low back pain clinically and lumbar IVD degeneration radiographically. The control group (N = 139) included subjects with and without low back pain; all were negative radiographically for lumbar IVD degeneration. Using PCR-RFLP analysis, we analyzed VEGF (-2578C>A, -1154G>A, -634G>C, and 936C>T) and eNOS (-786T>C, 4a4b and 894G>T) SNPs. We made combined analyses of the genes and performed haplotype analyses. There were no significant differences in the genotype distribution of polymorphisms of VEGF and eNOS genes among patients and controls. However, the frequency of VEGF -2578CA +AA/-634CC combined genotypes was significantly higher in patients when compared with controls [odds ratio (OR) = 21.00; 95% confidence interval (CI) = 2.590- 170.240]. The frequencies of the -2578A/-1154A/-634C/936C (OR = 3.831; 95%CI = 1.068-13.742), -2578A/-1154A/-634C (OR = 3.356; 95%CI = 1.198-9.400), and -2578A/-634C/936C (OR = 10.820; 95%CI = 2.811-41.656) haplotypes were also significantly higher in patients than in controls. We conclude that the combined genotype VEGF -2578CA+AA/-634CC is a possible risk factor for IVD degeneration and the VEGF -2578A/-1154A/-634C/936C haplotype may increase the risk for development of IVD degeneration. Furthermore, the VEGF -634C allele appears to be associated with susceptibility to IVD degeneration.

Endothelial Nitric Oxide Synthase Gene Polymorphism and the Risk of Diabetic Neuropathy in Asian Indian Patients with Type 2 Diabetes

Endothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease, including diabetic neuropathy (DNP). Endothelial-derived nitric oxide synthase (eNOS) gene polymorphisms affect eNOS activity and are associated with endothelial dysfunction. Studies examining association of eNOS gene polymorphism in type 2 diabetic patients (T2DM) with DNP and without DNP are lacking in Asian Indians. Thus, we investigated the association and interaction between two potentially functional single nucleotide polymorphisms (SNPs) of the eNOS gene (T-786C, G894T) and one repeat polymorphism (27VNTR) with DNP using validated PCR-RFLP assays in 1258 T2DM subjects belonging to two independent cohorts from north Indian Origin and also, we replicated our study in a 3rd independent cohort from south Indian population having T2DM. We also measured serum Nitric Oxide (NO) levels in these subjects and examined its correlation with DNP and eNOS genotypes. We observed that eNOS genotype carrying ‘aa’ genotype of 27VNTR (a/b) and eNOS haplotype C-a-G and C-a-T (allele of T-786C, 27VNTR a/b and G894T) carrying ‘a’ allele of 27VNTR (a/b) were associated with increased risk of DNP, in all the three cohorts. We also observed lower serum NO levels in T2DM subjects (both cases and controls) carrying ba+aa genotypes. Our study suggest that 27VNTR (a/b) eNOS polymorphism carrying ‘a’ allele alone and in association with T-786C and G894T eNOS polymorphism is associated with increased risk of DNP in Asian Indians T2DM patients.

Glu298Asp polymorphism influences the effects of beetroot bread on diastolic blood pressure in healthy men: A pilot study

Glu298Asp polymorphism of the endothelial nitric oxide synthase eNOS gene (NOS3) has previously been identified as a risk factor for hypertension and coronary artery disease. Studies suggest that the higher risk observed in thymine (T) allele carriers is due to endothelial dysfunction associated with lower eNOS activity. It has been proposed that acute consumption of nitrate ameliorates postprandial endothelial dysfunction possibly by the donation of nitric oxide by a mechanism that does not rely on eNOS. Nevertheless, how these factors interact has yet to be determined. Therefore, the aim of this study was to investigate whether the presence of NOS3 Glu298Asp polymorphism interacts with the nitrate content of beetroot-enriched bread to influence postprandial blood pressure.

The role of eNOS and AGT gene polymorphisms in secondary pulmonary arterial hypertension in Romanian children with congenital heart disease

The role of eNOS and AGT gene polymorphisms in secondary pulmonary arterial hypertension in Romanian children with congenital heart disease

Effect of eNOS polymorphisms on salbutamol evoked endothelium dependent vasodilation in South Indian healthy subjects

Background:The model of pulse plethysmograph using inhalational salbutamol 400 mcg is studied well to assess endothelium dependent vasodilation. Endothelial nitric oxide synthase (eNOS) gene polymorphism may influence the response to salbutamol in healthy subjects.Aim:To find the effect of polymorphisms 894G>T and -786T>C of eNOS gene on endothelium dependent vasodilation in healthy subjects.Materials and Methods:One hundred and two south Indian healthy subjects of either sex, aged between 18 to 35 years were recruited for the study. The digital volume pulse (DVP)was measured by pulse plethysmograph before and after salbutamol 400mcg inhalation. Three predose and five postdose recordings of DVP were measured. The average change in the DVP parameters namely reflection index (RI) and stiffness index (SI) were determined. The eNOS894G>T and -786T>C gene polymorphism were genotyped using polymerase chain reaction followed by restriction fragment length polymorphism. The percentage changes in RI and SI from predose baseline recordings were calculated and compared between the genotype groups.Results:The genotype and allele frequency of study subjects were in Hardy-Weinberg equilibrium. The changes in DVP parameters were not significantly different between the genotype groups.Conclusion:eNOS polymorphism do not affect salbutamol evoked endothelium dependent vasodilation in the model of pulse plethysmograph in healthy subjects.