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The Higher Frequency of G Allele Found in the -152 Site of Agt Gene But was Not Aligned with the Angiotensinogen Levels
Author(s) -
Akhiyan Hadi Susanto,
Mohammad Saifur Rohman
Publication year - 2018
Publication title -
international journal of pharmaceutical quality assurance
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.114
H-Index - 7
ISSN - 0975-9506
DOI - 10.25258/ijpqa.v9i01.11352
Subject(s) - allele , genotype , single nucleotide polymorphism , snp , allele frequency , genotype frequency , gene , essential hypertension , genetics , polymorphism (computer science) , biology , microbiology and biotechnology , medicine , endocrinology , blood pressure
Pathogenesis of essential hypertension involves an interaction between genetic and environmental factors. Genetic variant G-152A of angiotensinogen (AGT) promoter is thought to affect AGT gene transcription and angiotensinogen levels. Angiotensinogen is an important substrate for renin in the RAS that is finally converted into angiotensin II that plays a key role in the control of blood pressure. However, the studies that discuss the single nucleotide polymorphism (SNP) G-152A of AGT gene are still limited, especially in Indonesian hypertensive patients. Therefore, this study was designed to detect the SNP G-152A of AGT and reported its serum angiotensinogen levels. The variants were identified in 62 patients in Malang, Indonesia with essential hypertension by PCR and further identified by automated sequencing. Serum samples were collected to analyze the angiotensinogen levels by a sandwich ELISA. The data showed that the AGT promoter in our patients had genetic variants -152G (G allele/GG genotype) and -152A (A allele/AG genotype) with a frequency of 0.92 : 0.08, respectively. There were no patients with AA genotype. In the analysis of serum angiotensinogen levels (mean ± SD), it was found that A allele had an angiotensinogen level of 371.30 ± 69.92 (ng/mL) and G allele was 343.53 ± 74.95 (ng/mL). The A allele had slightly higher angiotensinogen level than G allele with no significant difference (P=0.437). Thus, in our study is found a genetic variant G-152A of AGT gene represented the GG, AG genotypes in the (-152) site and it has higher frequency of G allele. Further research is still needed to determine that G/A allele directly affects on the occurrence of essential hypertension.

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