Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/6550
Title: Relationship between hemorheology and Glu(298)Asp polymorphism of endothelial nitric oxide synthase gene in patients with coronary artery disease
Authors: Bor-Küçükatay, Melek
Demir, Süleyman
Akbay, R.
Dursunoglu, Dursun
Akdağ, Beyza
Semiz, E.
Keywords: Cardiovascular risk
Coronary artery disease
Hemorheology
Nitric oxide synthase
Polymorphism
aspartic acid
endothelial nitric oxide synthase
glutamic acid
nitrate
nitrite
adult
aged
allele
article
blood rheology
blood viscosity
cardiovascular risk
controlled study
coronary artery disease
cytometry
erythrocyte aggregation
erythrocyte deformability
female
gene frequency
genetic polymorphism
genotype
human
major clinical study
male
plasma viscosity
restriction fragment length polymorphism
viscometer
Adult
Aged
Aged, 80 and over
Alleles
Amino Acid Substitution
Aspartic Acid
Case-Control Studies
Coronary Artery Disease
Electrophoresis, Agar Gel
Erythrocyte Aggregation
Female
Gene Frequency
Genotype
Glutamic Acid
Humans
Male
Middle Aged
Nitric Oxide Synthase Type III
Polymorphism, Single Nucleotide
Abstract: This study aimed to investigate the relationship between endothelial nitric oxide synthase Glu(298)Asp gene polymorphism and hemorheological parameters. Red blood cell (RBC) deformability, aggregation were measured using an ectacytometry, whole blood, plasma viscosities were determined by a viscometer. Restriction fragment length polymorphism was used to detect polymorphism. Plasma nitrite, nitrate concentrations were determined by Griess method. The genotype distribution of the control group was as follows: 50 (67.5%) GG, 21 (28.4%) GT, 3 (4.1%) TT. A 48 (57.8%) of the patients with CAD had GG, 28 (33.7%) GT, 7 (8.5%) of them TT genotype. RBC aggregation index of CAD patients with G allele was higher and t1/2 lower compared to controls carrying the same allele. The amplitude of RBC aggregation of healthy subjects with T allele, who are under increased cardiovascular risk was lower compared to control subjects with G allele. The results of this study indicate that, alterations in RBC aggregation seem to be a consequence of CAD, more than being a preexisting cause. Additionally, some compensatory mechanisms by causing decrements in RBC aggregation, may help regulation of circulation in healthy individuals with high cardiovascular risk. © 2009 Springer Science+Business Media B.V.
URI: https://hdl.handle.net/11499/6550
https://doi.org/10.1007/s11033-009-9572-9
ISSN: 0301-4851
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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