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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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