Furthermore, compared with the MI group, the plasma levels of TXA2, ET-1 and vWF contents signififi cantly decreased in the MI+SSYX group, and the ET-1 mRNA expression levels of myocardium in the border zone significantly decreased, and the VEGF, PGI2 and eNOS mRNA expression levels signififi cantly increased (all P<0.05).
Homozygosity for a common NOS 3 polymorphism (894 G-->T) which encodes a Glu298-->Asp amino acid substitution in eNOS is a risk factor for angiographic CAD and recent MI in this population.
We hypothesized that the NOS3 synthase 4a4b VNTR polymorphism is a determinant of tHcy concentrations and tested this in 310 patients with MI and 250 controls.
We have identified a missense variant, Glu298Asp, in exon 7 of the eNOS gene and demonstrated that it is associated with both coronary spastic angina and myocardial infarction.
There appeared to be a significant difference in the genotype and allele distribution of eNOST-786C polymorphism between T2DM groups with and without CAD (p=0.004), albeit no significant association with MI was observed.
This study explored whether pravastatin decreases myocardial infarct size and this effect is associated with endothelial nitric oxide synthase (eNOS) expression in myocardium.
To determine whether the polymorphic dinucleotide repeats found in intron 4 of the endothelial cell nitric oxide synthase (ecNOS) gene and the platelet GPIIIa PLA(1)/A(2) polymorphism are associated with myocardial infarction (MI) and venous thromboembolism (VTE) in African Americans.
We have identified polymorphisms in the NOS 3 gene and one of these polymorphisms, Glu(298-->)Asp, was found to be a major risk factor for carotid artery disease and myocardial infarction.
We have explored a set of polymorphisms of the ecNOS gene in a large case-control study of MI and found that the polymorphisms were not consistently associated with MI.
Recently, a Glu298Asp variant of the endothelial nitric oxide synthase gene (NOS3) was identified as being associated with coronary spasm and myocardial infarction, whereas it has been reported that endothelial nitric oxide synthase plays a role in HP.
An endothelial nitric oxide synthase gene (NOS3) polymorphism in exon 7 (G894T), resulting in Glu298Asp substitution at protein level, has been associated with myocardial infarction, hypertension and coronary atherosclerosis in some populations.
This finding implies that genetic polymorphism G894T on eNOS may affect endothelial function in patients with a history of premature myocardial infarction.
Cases (all-cause death, nonfatal myocardial infarction (MI), or nonfatal stroke) and an age-, sex-, race/ethnicity-matched control population were genotyped for the -786T>C and Glu298>Asp polymorphisms in NOS3.
The aim of this study was an assessment of association of human endothelial nitric oxide synthase gene Ban II polymorphism with the myocardial infarction in 178 patients and 136 healthy individuals.
In the present study, we examined a possible association between a 27-base pair (bp) repeat polymorphism in intron 4 of the NOS3 gene and MI in a subgroup of the Tunisian population.
Exercise Training Has Contrasting Effects in Myocardial Infarction and Pressure Overload Due to Divergent Endothelial Nitric Oxide Synthase Regulation.
On the other hand, intriguingly, genetic disruption of all three nitric oxide synthase (NOS) isoforms (neuronal NOS, inducible NOS, and eNOS) spontaneously caused MI accompanied by multiple cardiovascular risk factors of metabolic origin in mice.
Pooled odds ratios (OR) with 95% confidence interval (CI) were calculated to evaluate the association of eNOS gene T-786C and 4b4a polymorphisms with MI risk.
Consequently, we first tested the hypothesis that the effects of exercise after MI can be mimicked by elevated eNOS expression using transgenic mice with overexpression of human eNOS (eNOSTg).
Results showed reduced endothelial nitric oxide synthase (eNOS) protein expression in the MI group; increased iNOS activity in the HgCl<sub>2</sub>-MI group, although without enough magnitude to reverse the reduction in NO bioavailability; and increased phenylephrine response in the HgCl<sub>2</sub>-MI group due to an increase in ROS production, notably via xanthine oxidase (XO).