Endothelial Nitric Oxide Synthase Glu298Asp Research Articles

Association of endothelial nitric oxide synthase (Glu298Asp) gene polymorphism with radial artery spasm during cardiac catheterization in Egyptians

BackgroundNitric oxide (NO) exerts diverse effects on the cardiovascular system. Impairment of NO production plays a key role in cerebral and coronary artery spasm. We aimed to explore the predicting factors of radial artery spasm (RAS) and the association of eNOS gene polymorphism (Glu298Asp) with RAS during cardiac catheterization.Methods and results200 patients underwent elective coronary angiography through a trans-radial approach. The subjects were genotyped to the Glu298Asp polymorphism (rs1799983) on the eNOS gene by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Our results showed that the subjects with the TT genotype and T allele were significantly more likely to develop radial artery spasms (OR = 12.5, 4.6, P < 0.001 respectively). TT genotype of eNOS Glu298Asp polymorphism, number of punctures, size of the radial sheath, radial tortuosity, and right radial access are independent predictors of radial spasm.ConclusionThe eNOS (Glu298Asp) gene polymorphism is associated with RAS during cardiac catheterization in Egyptians. TT genotype of eNOS Glu298Asp polymorphism, number of punctures, size of the radial sheath, right radial access, and tortuosity are independent predictors of RAS during cardiac catheterization.

Endothelial nitric oxide synthase Glu298Asp gene polymorphism in the cases of idiopathic thrombocytopenic purpura.

BackgroundNitric oxide (NO) can induce apoptosis in megakaryocytes. Stimulatory function of NO on platelet production may be important in the pathophysiology of idiopathic thrombocytopenic purpura (ITP). NO is produced by three isoforms of NO synthase (NOS). The endothelial nitric oxide synthase (eNOS) isoform has been detected in platelets. Polymorphism of the eNOS gene, which supplies NO synthesis, changes the functions of this enzyme. In this study, the role of eNOS Glu298Asp gene polymorphism in etiopathogenesis, its course, and treatment of ITP was investigated.MethodsSixty-six patients [51 newly diagnosed ITP (ND-ITP), 15 chronic ITP (CH-ITP), and 60 healthy controls (HC)] were enrolled in this study.ResultsIn all patients, the frequency of the GT genotype was 48.5%. The frequency of the GG genotype was determined to be 40.9% and the TT genotype was 10.6%. The most common allele in all patients was the G allele. eNOS Glu298Asp gene polymorphism might be a risk factor in the etiopathogenesis of ITP. Patients with the GG genotype were thought to have a high intention for CH-ITP. Patients with the GG genotype responded effectively to medical treatment using IVIG therapy. The presence of the G allele was observed to have a positive effect on the medical treatment of patients with CH-ITP, whereas the T allele exhibited a negative effect.ConclusionIn the present study, a significant correlation was found between ITP and eNOS Glu298Asp gene polymorphism. This correlation suggested that eNOS Glu298Asp gene polymorphism might be a risk factor in the ethiopathogenesis of ITP.

Endothelial nitric oxide synthase (Glu298Asp) polymorphism is associated significantly with ischemic stroke presenting with seizures and altered sensorium

Endothelial nitric oxide synthase (eNOS) is an enzymatic marker whose genetic polymorphism might predispose to acute ischemic stroke (AIS) via vascular endothelial dysfunction. It has potential role in atherosclerosis, making it a plausible risk factor for stroke. Prior studies have failed to prove a conclusive relationship between eNOS polymorphism and AIS. The aim of this study is to find an association between the presence of eNOS polymorphism (Glu298Asp) and the risk of developing AIS.

Асоціація поліморфізму гена ендотеліальної синтази оксиду азоту (Glu298Asp) із хронічною серцевою недостатністю у хворих на ішемічну хворобу серця й ожиріння

У статті оцінено наявність зв’язків між поліморфізмом гена ендотеліальної синтази оксиду азоту (Glu298Asp) і розвитком та прогресуванням хронічної серцевої недостатності у хворих на ішемічну хворобу серця й ожиріння. Було проведено комплексне обстеження 222 хворих на ішемічну хворобу серця. Групу порівняння становили 115 хворих на ішемічну хворобу серця з нормальною масою тіла. До конт­рольної групи увійшло 35 практично здорових осіб. Алель G і генотип G/G поліморфізму гена ендотеліальної синтази оксиду азоту (Glu298Asp) були асоційовані з розвитком ішемічної хвороби серця. Наявність алелі G та генотипу G/G поліморфізму гена ендотеліальної синтази оксиду азоту (Glu298Asp) у хворих на ішемічну хворобу серця із супутнім ожирінням була пов’язана з розвитком хронічної серцевої недостатності, тоді як алель А була пов’язана зі зниженням ризику розвитку серцевої недостатності. Прогресування хронічної серцевої недостатності у хворих на ішемічну хворобу серця й ожиріння асоціювалось з алеллю G поліморфізму гена ендотеліальної синтази оксиду азоту (Glu298Asp), а алель А мала захисні властивості.

Endothelial Nitric Oxide Synthase (Glu298Asp) Polymorphism Is Associated Significantly With Ischemic Stroke Presenting With Seizures And Altered Sensorium (4961)

Endothelial Nitric Oxide Synthase (Glu298Asp) Polymorphism Is Associated Significantly With Ischemic Stroke Presenting With Seizures And Altered Sensorium (4961)

Endothelial Nitric Oxide Synthase (Glu298Asp) Polymorphism is Associated Significantly with Ischemic Stroke Presenting with Seizures and Altered Sensorium.

Endothelial nitric oxide synthase (eNOS) is an enzymatic marker whose genetic polymorphism might predispose to acute ischemic stroke (AIS) via vascular endothelial dysfunction. It has a potential role in atherosclerosis, making it a plausible risk factor for stroke. Prior studies have failed to prove a conclusive relationship between eNOS polymorphism and AIS. The aim of this study is to find an association between the presence of eNOS polymorphism (Glu298Asp) and the risk of developing AIS. We recruited 307 subjects including 153 AIS cases and 154 healthy controls. The eNOS (Glu298Asp) polymorphism was identified in EDTA blood by PCR amplification of the target region followed by restriction enzyme digestion, and genotyping on Agarose gel. GG, GT and TT genotypes were obtained. Statistical analysis was done using SPSS software version 20. A significant association was found between the presence of TT genotype and the risk of AIS (Odd's ratio (OR): 2.43, P-value = 0.038). There was no significant association between the TT genotype and the traditional stroke risk factors. However, the TT genotype was significantly associated with the presence of altered consciousness (OR: 5.27, 95% CI: 1.59-17.04, P-value = 0.003) and with the occurrence of seizures at presentation (OR: 7.98, 95% CI: 1.99-32.09, P-value = 0.007). There is a significant association between the presence of eNOSpolymorphism (Glu298Asp) and the risk of AIS, and the TT genotype may predispose to a more severe initial presentation of ischemic stroke.

Association between Endothelial Nitric Oxide Synthase Gene Polymorphism (Glu298Asp) and Coronary No-Reflow Phenomenon in Acute Myocardial Infarction

No-reflow phenomenon is an important complication of primary percutaneous coronary intervention. Several variants in the endothelial nitric oxide synthase gene, which reduce endothelial nitric oxide synthase activity, are a risk factor for coronary heart disease. However, its role in no-reflow phenomenon has not yet been revealed. This study aimed to investigate whether there is a relationship between endothelial nitric oxide synthase Glu298Asp gene variant and the development of coronary no-reflow phenomenon in patients with ST elevation myocardial infarction. The study was conducted among 116 patients undergoing primary percutaneous coronary intervention for ST elevation myocardial infarction. Group 1 included 52 ST elevation myocardial infarction patients undergoing no-reflow phenomenon as a study group. Group 2 comprised 64 ST elevation myocardial infarction patients without no-reflow phenomenon as a control group. Endothelial nitric oxide synthase was tested using polymerase chain reaction-restriction fragment length variant. The prevalence of TT genotype of endothelial nitric oxide synthase Glu298Asp gene variant was found to be significantly higher in patients developing coronary no-reflow when compared to those without no-reflow (p = 0.016; 11.54% vs. 1.56%) (OR = 10.85, 95% CI = 1.22–96.39). However, a similar association for the heterozygous GT genotype of endothelial nitric oxide synthase Glu298Asp gene variant was not observed between the two groups. The results of this preliminary study indicate that there is an association between Glu298Asp variant in endothelial nitric oxide synthase gene and the development of no-reflow phenomenon in ST elevation myocardial infarction. The presence of homozygous TT allele may contribute to tendency to the development of no-reflow phenomenon.

ACUTE VASODILATOR TESTING: AN OPPORTUNITY TO REFINE STUDY DESIGN AND PROVIDE PRECISION CARE IN PULMONARY HYPERTENSION

SESSION TITLE: Pulmonary Vascular Disease SESSION TYPE: Fellow Case Reports PRESENTED ON: 10/07/2018 10:45 AM - 11:45 AM INTRODUCTION: Inhaled nitric oxide is currently used to acutely evaluate pulmonary vascular reactivity and identify patients with pulmonary arterial hypertension who may be appropriate candidates for long-term treatment with a calcium channel blocker (CCB). However, some patients with an acute decrease in mean pulmonary arterial pressure (MPAP) with nitric oxide fail to improve, or progressively worsen over time, with a CCB alone. Here we present a patient with severe pulmonary arterial hypertension who develops a normal MPAP while breathing nitric oxide. We describe the acute and long-term effects of other agents on her MPAP. CASE PRESENTATION: The patient presented at 8 years of age in 2003 with decreased exercise tolerance and syncope. Non-invasive studies were consistent with a diagnosis of idiopathic pulmonary arterial hypertension. Her hemodynamic measurements during heart catheterization and acute vasodilator testing are shown along with interim therapy in the table. See tableThe patient's MPAP has consistently decreased to normal during acute vasodilator testing with nitric oxide. There was little or no acute improvement in MPAP with nitroglycerin and sildenafil, and a corresponding failure with therapy long-term. There was moderate acute improvement with diltiazem and riociguat, and a corresponding moderate improvement with amlodipine long-term. The dose of amlodipine and the dose of riociguat have been limited by adverse side effects (gingival hyperplasia and gastroesophageal reflux). Nighttime nitric oxide therapy was safely used in her home for 4 months when an increase in MPAP was temporally associated with an adverse reaction to minocycline. Unfortunately, a reliable delivery system was not available to continue long-term therapy at that time.She has a polymorphism in endothelial nitric oxide synthase (Glu298Asp), a normal cytogenomic microarray and elevated levels of asymmetric dimethylarginine. Genetic testing for specific variants associated with pulmonary arterial hypertension has not been performed. DISCUSSION: Our patient's response to nitric oxide is consistent with a phenotype of decreased endothelial nitric oxide synthase function. Her clinical course illustrates how acute vasodilator testing may be used to guide therapy, even if a corresponding genotype is unknown. In this case, long-term inhaled nitric oxide may be more effective and less likely to cause adverse systemic effects than other agents. Any agent may fail to demonstrate a beneficial effect in a heterogeneous population of patients, but may have a meaningful effect in a subset of responsive patients. For example, a combination of inhaled nitric oxide and a CCB might prevent long-term treatment failures that occur with a CCB alone. CONCLUSIONS: Acute vasodilator testing identified appropriate medications for the long-term therapy of our patient. There is a need to design trials with a focus on precision care. Reference #1: Day, RW. Differences in the acute pulmonary vascular effects of oxygen with nitric oxide and diltiazem: Implications for the long-term treatment of pulmonary arterial hypertension. Congenit Heart Dis 2013;8:71-77. DISCLOSURES: No relevant relationships by Meghan Cirulis, source=Web Response No relevant relationships by Nicole Day, source=Web Response No relevant relationships by Ronald Day, source=Web Response No relevant relationships by Lynda Jorgensen, source=Web Response

Endothelial Nitric Oxide Synthase (eNOS) Glu298Asp Gene Polymorphism (G894T) as a Risk Factor for Type 2 Diabetes Mellitus in the Tunisian Population

Introduction: Diabetes mellitus is a chronic disease whose global expansion gives it the characteristics of a pandemic. Diabetes risk factors are well known. In this work we proposed to study the role of genetic polymorphism of the eNOS G894T gene in the development of diabetes on the one hand and of these degenerative complications other. Methods: We conducted a prospective case-control study in which we included 200 subjects divided into 100 patients with type 2 diabetes and 100 controls in apparent good health. For each patient and control we measured lipid parameters, CRP-us and sought the G894T polymorphism of eNOS gene by PCR-RFLP. Results: The analysis of our results shows a statistically significant elevated TG values (p < 10﹣3), Lp (a) (p < 10﹣3), and CRP-us (p < 10﹣3) in type 2 diabetes compared with controls. The mutated genotypes of GT eNOS gene was significantly more frequent in diabetic patients. In our series, we did not notice any significant difference in genotype or allele frequency between diabetics with and without degenerative complications. Conclusion: The G894T polymorphism of eNOS gene appears to be a risk factor of T2DM. His role in the development of degenerative complications remains proved.

Endothelial nitric oxide synthase Glu298Asp gene polymorphism influences body composition and biochemical parameters but not the nitric oxide response to eccentric resistance exercise in elderly obese women

Both endothelial nitric oxide synthase (eNOS) gene polymorphism and nitric oxide (NO) are involved in important cardiovascular, muscular and inflammatory physiological mechanisms during ageing and response to exercise. The aim of this study was to investigate the NO kinetic response following an acute eccentric resistance exercise (ERE) session and the possible effect of the Glu298Asp eNOS gene polymorphism in elderly obese women. Eighty-seven women (age 69·4±6·1years, body weight 74·9±12·7kg, height 151·9±6·0cm and BMI 32·5±5·7kgm-2 ) completed seven sets of ten eccentric repetitions at 110% of the ten repetitions maximum (10RM). NO concentrations remained elevated up to 48h following the acute ERE session as compared with baseline, for GG and GT/TT groups (P<0·05), with no differences between genotypes. The GG genotype group had higher body weight, prevalence of obesity (BMI classification - 81% versus 56%), BMI and higher relative muscle strength, while they had significantly lower triglycerides, VLDL and urea concentrations as compared with TT/TG group. In conclusion, NO remains elevated for up to 48h after an acute ERE session, without genotype interaction. The TT/TG genotype had a negative impact on triglycerides, VLDL and urea concentrations. Thus, T carriers should increase their attention to cardiovascular risk factor and metabolic disorders.

Association of endothelial nitric oxide synthase Glu298Asp gene polymorphism in psoriasis cases with hypertension.

BACKGROUND AND OBJECTIVESPsoriasis is a common autoimmune-mediated chronic, inflammatory skin disease. Although, the molecular mechanism is not completely understood, psoriasis is caused by genetic and non-genetic parameters. The current study aimed (1) to define genotype and allele frequency of endothelial nitric oxide synthase (eNOS Glu298Asp) gene polymorphism in hypertensive and/or non-hypertensive psoriatic patients (2) to investigate the possible relationship between the eNOS Glu298Asp polymorphism and the risk of hypertension among psoriatic patients in the Turkish population.DESIGN AND SETTINGSThis cross-sectional, case-control study was performed between March 2010 and November 2012 at the University hospital in Çanakkale, TurkeyPATIENTS AND METHODSGene profiles of 75 psoriatic patients (21 hypertensive and 54 normotensive patients) and 55 healthy (normotensive and non-psoriatic) volunteers were compared. Peripheral blood-EDTA samples were used for total genomic DNA isolation and genotyping. Target eNOS gene was genotyped for patients and control groups by real-time PCR melting-curve analysis system (LightCycler 2.0, Roche, Germany, and results were compared statistically.RESULTSAn increased T allele frequency in eNOS Glu298Asp single-nucleotide polymorphism (SNP) was determined in psoriatic patients when compared with normotensive non-psoriatic healthy volunteers (OR 2.3, CI 1.14–3.99), (P=.017). The T allele frequency was also found to be increased in hypertensive psoriatic patients when compared with healthy volunteers (4.83-fold increased, 95% CI 1.62–14.43 ([P=.003]) and normotensive psoriatic patients (3.03-fold increased, 95% CI 1.03–8.94 [P=.041]), respectively.CONCLUSIONThe current preliminary results suggested that there was a correlation between eNOS Glu298Asp polymorphism and hypertension among psoriatic patients in the Turkish population. The T allele frequency of eNOS Glu298Asp SNP was different in hypertensive psoriatic patients, and the difference was statistically significant when compared with the normotensive psoriatic patients and healthy controls. These results need to be confirmed by large-scale studies.

OP-334 Association between Coronary No-Reflow Phenomenon and Endothelial Nitric Oxide Synthase (Glu298Asp) Gene Polymorphism

The aim of the present study was to demonstrate, through the analysis of novel parameter like PON1, that early changes in oxidative stress takes place in stable coronary artery disease (CAD) patients undergoing elective PCI with implantation of coronary stents. Methods: In this study 32 consecutive chronic stable angina patients (mean age 61 9.8 years, 75% male) undergoing PCI for management of single-vessel CAD (>70% stenosis in a major coronary artery) were included. PON1 enzyme activity were measured immediately before (t1) and just after the procedure (t2), as well as 24 hours later (t3), in order to serially evaluate the changes of oxidative stress parameters in PCI. Results: Baseline demographic, clinical and laboratorycharacteristics of the patients were demonstrated Table 1. When PON1 activities before (t1), immediately after (t2) and 24 hours after (t3) PCI procedurewere compared, a sustained decline was demonstrated (t3 t2 and t3, p 0.05, respectively). There was no correlation between serum PON1 activity and clinical and laboratory parameters of patients. Conclusion: We demonstrated, for the first time, that a substantial impairment of PON1 activity occurs after PCI in patients with stable CAD.We suggest that the PON1 assay may have the potential to be used as an early risk predictor for restenosis in patients undergoing elective PCI with implantation of BMS, a hypothesis which requires further studies.

Synergistic effect of androgen receptor (CAG repeat length) and endothelial nitric oxide synthase (Glu298Asp variant) gene polymorphisms on seminal parameters in men with idiopathic oligoasthenozoospermia

Synergistic effect of androgen receptor (CAG repeat length) and endothelial nitric oxide synthase (Glu298Asp variant) gene polymorphisms on seminal parameters in men with idiopathic oligoasthenozoospermia

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.

Association of Endothelial Nitric Oxide Synthase Glu298Asp Gene Polymorphism with the Risk of End-Stage Renal Disease

The association between endothelial nitric oxide synthase (eNOS) Glu298Asp gene polymorphism and end-stage renal disease (ESRD) risk is still controversial. A meta-analysis was performed to evaluate the association between eNOS Glu298Asp gene polymorphism and ESRD susceptibility. A predefined literature search and selection of eligible relevant studies were performed to collect data from electronic database. Six articles were identified for the analysis of association between eNOS Glu298Asp gene polymorphism and ESRD risk. T allele was associated with ESRD susceptibility in overall populations and in Asians (overall populations: p = 0.01, Asian: p < 0.00001). Furthermore, GG genotype might play a protective role against ESRD onset for overall populations, Asians, and Africans. However, a link between eNOS Glu298Asp gene polymorphism and ESRD risk was not found in Caucasians and Brazil population. In conclusion, T allele might become a significant genetic molecular marker for the onset of ESRD in overall populations, and in Asians. However, more studies should be performed in the future.

Correlation of Glu298Asp eNOS Polymorphism with Serum NO Levels in Egyptian Patients with Coronary Artery Disease

Background: Nitric oxide (NO) is a potent vasodilator synthesized by the vascular endothelium. It has been reported that endothelial nitric oxide synthase (eNOS) Glu298Asp gene polymorphism is associated withcoronary artery disease (CAD). Methodology: In this study, we investigated Glu298Asp eNOS polymorphism and serum NO in a group of 146 age-matched male subjects; 77 patients with coronary artery disease (CAD) classified according to the severity of coronary insufficiency and 69 normal male controls. Results: The obtained frequencies of the eNOS Glu298Asp genotypes for the CAD subjects were GG (54.5%), GT (31.20%), and TT (14.3%).The allele distributions of G and T were 70.1 and 29.9%, respectively. In the control group, the genotype frequencies were 53.6% for GG, 36.2% for GT, and 10.2% for TT, and the frequencies of the G and T alleles were 71.7% and 28.3%, respectively. There we re no significant differences in genotype and allele frequencies between the CAD patients and the control group. The mean serum NO levels in CAD patients was significantly higher than that of healthy subjects (p=0.0139). Conclusion: No significant associa tion was detected when CAD severity, genotypes and NO serum levels were correlated.

Endothelial Nitric Oxide Synthase Glu298Asp Polymorphism as a Risk Factor for Prostate Cancer

The endothelial form of nitric oxide synthases (eNOS) seems to have an important role in vascular development, maintenance of the vascular tone and tumor growth in human prostate cancer (PC). The purpose of this study was to investigate the association between grade and stage of disease, age of diagnosis, vascular or perineural invasion, pre-diagnostic plasma prostate-specific antigen (PSA) levels, prostate cancer risk and Glu298Asp polymorphism of the eNOS gene. Ninety-five prostate cancer patients and 111 benign prostate hyperplasia subjects were included. The Glu298Asp polymorphism of the eNOS gene was determined by polymerase chain reaction and restriction fragment length polymorphism The odds ratio (OR) between the GT and GG polymorphism was 0.76, indicating that the presence of the GT polymorphism decreased the risk of prostate cancer of more than 20% compared to the GG polymorphism. This difference, however, was not statistically significant. The GT polymorphism had an inverse association with cancer grade compared to the reference group (OR=0.47, p value=0.2). These results suggest that prostate cancer development is not associated with the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in our population. Further studies in larger samples are needed to confirm our results and characterize the molecular mechanisms by which eNOS is involved in the susceptibility to prostate cancer.

Association between Endothelial Nitric Oxide Synthase Glu298Asp Gene Polymorphism and Diabetic Nephropathy Susceptibility

The association between endothelial nitric oxide synthase (eNOS) Glu298Asp gene polymorphism and diabetic nephropathy (DN) risk is still controversial. A meta-analysis was performed to evaluate the association between eNOS Glu298Asp gene polymorphism and DN susceptibility. A predefined literature search and selection of eligible relevant studies were performed to collect data from electronic database. Eight articles were identified for the analysis of association between eNOS Glu298Asp gene polymorphism and DN risk. T allele was associated with DN susceptibility in overall populations, in Asians, and for Caucasians (overall populations, p = 0.005; Asians, p = 0.004; Caucasians, p = 0.002). Furthermore, GG genotype might play a protective role against DN onset for overall populations, Asians, Caucasians, and Africans. However, a link between eNOS Glu298Asp gene polymorphism and DN risk was not found in overall populations, Asians, Caucasians, and Brazil population. In conclusion, T allele might become a significant genetic molecular marker for the onset of DN in overall populations, in Asians, and for Caucasians. However, more studies should be performed in the future.

Glu298Asp polymorphism influences the beneficial effects of fish oil fatty acids on postprandial vascular function

Our objective was to determine whether the endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism influences vascular response to raised NEFA enriched with saturated fatty acids (SFA) or long-chain (LC) n-3 polyunsaturated fatty acids (PUFA). Subjects were prospectively recruited for genotype (Glu298, n = 30 and Asp298, n = 29; balanced for age and gender) consumed SFA on two occasions, with and without the substitution of 0.07 g fat/kg body weight with LC n-3 PUFA, and with heparin infusion to elevate NEFA. Endothelial function was measured before and after NEFA elevation (240 min), with blood samples taken every 30 min. Flow-mediated dilation (FMD) decreased following SFA alone and increased following SFA+LC n-3 PUFA. There were 2-fold differences in the change in FMD response to the different fat loads between the Asp298 and Glu298 genotypes (P = 0.002) and between genders (P < 0.02). Sodium nitroprusside-induced reactivity, measured by laser Doppler imaging with iontophoresis, was significantly greater with SFA+LC n-3 PUFA in all female subjects (P < 0.001) but not in males. Elevated NEFA influences both endothelial-dependent and endothelial-independent vasodilation during the postprandial phase. Effects of fat composition appear to be genotype and gender dependent, with the greatest difference in vasodilatory response to the two fat loads seen in the Asp298 females.

Endothelial Nitric Oxide Synthase (G894T) Gene Polymorphism in a Random Sample of the Egyptian Population: Comparison with Myocardial Infarction Patients

The aim of this study was to detect endothelial nitric oxide synthase (eNOS) Glu298Asp gene variants in a random sample of the Egyptian population, compare it with those from other populations, and attempt to correlate these variants with serum levels of nitric oxide (NO). The association of eNOS genotypes or serum NO levels with the incidence of acute myocardial infarction (AMI) was also examined. One hundred one unrelated healthy subjects and 104 unrelated AMI patients were recruited randomly from the 57357 Hospital and intensive care units of El Demerdash Hospital and National Heart Institute, Cairo, Egypt. eNOS genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Serum NO was determined spectrophotometrically. The genotype distribution of eNOS Glu298Asp polymorphism determined for our sample was 58.42% GG (wild type), 33.66% GT, and 7.92% TT genotypes while allele frequencies were 75.25% and 24.75% for G and T alleles, respectively. No significant association between serum NO and specific eNOS genotype could be detected. No significant correlation between eNOS genotype distribution or allele frequencies and the incidence of AMI was observed. The present study demonstrated the predominance of the homozygous genotype GG over the heterozygous GT and homozygous TT in random samples of Egyptian population. It also showed the lack of association between eNOS genotypes and mean serum levels of NO, as well as the incidence of AMI.