Abstract
Purpose: To investigate the distribution of methionine synthase A2756G (MSA2756G) in the hypertensive patients in northwest Chinese population.Methods: A total of 378 unrelated hypertensive patients attending Ningxia Peoples Hospital, Ningxia Province, China, were recruited for this study. We analyzed genotype by amplication - created restriction sites (ACRS) and polymerase chain reaction - restrict fragment length polymorphism (PCR - RFLP) in hypertensive patients, and inspected the relation of the genotype with hypertension by χ2 and t test.Results: The frequency of G allele was 10.25 % in the control group and 14.04 % in hypertension group; it was not statistically different (p > 0.05). In the male group, the frequency of allele G was 11.50 % in control group, and 8.79 % in hypertension group. There was no significant difference between control and hypertension groups (p > 0.05). In the female group, the frequency of allele G was 9.00 %, in control and 19.54 % in hypertension group (p < 0.05), while in the hypertension group, allele G was 8.79 % in males which is significantly lower (p < 0.05) than in females (19.54 %) .Conclusion: Allele G of MSA2756G is a risk factor for hypertension in female in this Chinese population of this study.Keywords: Hypertension, Methionine synthase, Polymorphism, Gender, Amplification-created restriction sites, Allele G, MSA2756G
Highlights
Hypertension is a major global public health problem due to its high prevalence and its association with morbidity and mortality from stroke and coronary diseases [1,2]
The subjects were adequately matched for age and gender for hypertensive cases and controls
The following variables were significantly higher in hypertensive patients: systolic blood pressure (SBP), diastolic blood pressure (DBP)
Summary
Hypertension is a major global public health problem due to its high prevalence and its association with morbidity and mortality from stroke and coronary diseases [1,2]. High blood pressure is regarded as a complex condition to which genetic, environmental, and demographic factors contribute interactively [4]. An enhanced function of MS will lead to a decreased plasma Hcy level. An A - to - G substitution of the MS gene (MSA2756G), which results in the conversion of an aspartic acid residue to a glycine residue, was found to play a role in regulating plasma Hcy levels [5]. Hcy was found to be associated with blood pressure levels in several studies [58]. In the light of these findings, MS gene polymorphism might be a possible underlying mechanism in blood pressure
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