Frequency of angiotensin-converting enzyme gene polymorphism in Turkish hypertensive patients

Abstract

Hypertension is a multifactorial disease, in which genetic factors play an important role. This study was carried out to determine angiotensin-converting enzyme levels and angiotensin-converting enzyme gene polymorphism in Turkish hypertensive patients, and to establish whether there is an association of angiotensin-converting enzyme gene polymorphism with clinical and echocardiographic parameters. We have investigated the association among the allelic distribution of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene identified by polymerase chain reaction, angiotensin-converting enzyme activity determined spectrophotometrically, cardiac morphology and function assessed by means of echocardiography. Distribution of angiotensin-converting enzyme gene I/D polymorphism and allele frequencies in hypertensive patients was not significantly different from controls. D allele frequency was 51.7% in hypertensives vs. 51.9% in controls and I allele 48.3 vs. 48.1%, respectively. The level of angiotensin-converting enzyme activity was significantly higher in the patients homozygotes for D allele (DD = 59.93 U/l) than in heterozygotes (ID = 39.49) and in homozygotes for I allele (II = 40.28 U/l). In addition to these, the level of angiotensin-converting enzyme activity was significantly lower in the ID and especially II patients receiving ACE inhibitors than the others. Also, it was determined that left atrium diameter was larger in the patients homozygotes for I allele than the others.

Association between I/D polymorphism in the ACE gene and sarcoidosis in Turkish patients

“…The DNA of each individual was isolated from the blood samples using the salt method as previously described (Gunes et al 2004). As described in the same study, amplification of the DNA samples was performed using the sense oligonucleotide primer 5 0 CTG CAG ACC ACT CCC ATC CTT TCT 3 0 and the antisense oligonucleotide primer 5 0 GAT GTG GCC ATC ACA TTC GTC AGA T 3 0 designed to detect ACE I/D polymorphism (Gunes et al 2004).…”

“…The DNA of each individual was isolated from the blood samples using the salt method as previously described (Gunes et al 2004). As described in the same study, amplification of the DNA samples was performed using the sense oligonucleotide primer 5 0 CTG CAG ACC ACT CCC ATC CTT TCT 3 0 and the antisense oligonucleotide primer 5 0 GAT GTG GCC ATC ACA TTC GTC AGA T 3 0 designed to detect ACE I/D polymorphism (Gunes et al 2004). One hundred nanograms of genomic DNA samples was amplified by 30 cycles of denaturation at 92°C for 40 s, annealing at 56°C for 40 s and extension at 72°C for 40 s, using a 50 ll of PCR mixture containing 10 pmol of each primer, 19 PCR buffer (Vivantis Technologies, Selangor, Malaysia) with magnesium chloride, 2.5 mM dNTPs, and 1.25 U of thermostable Taq polymerase (Vivantis Technologies).…”

“…I/D polymorphism in the ACE gene affects the ACE enzyme level in metabolic diseases like hypertension and sarcoidosis (Gunes et al 2004;Furuya et al 1996;Tomita et al 1997;Biller et al 2009). Therefore, the ACE genotype might be a genetic marker (Furuya et al 1996;Tomita et al 1997;Biller et al 2009;Papadopoulos et al 2000;Sharma and Alam 1995;Salobir et al 2007;Tahir et al 2007).…”

Is there any genetic predisposition of MMP-9 gene C1562T and MTHFR gene C677T polymorphisms with essential hypertension?

“…However, pathogenesis of hypertension is not clearly known (Gunes et al 2004;Bayramoglu et al 2012). Recently, the application of genetic approaches to this disease has begun to delineate molecular pathways underlying blood pressure variation, defining disease pathogenesis and identifying targets for therapeutic intervention.…”

“…Recently, the application of genetic approaches to this disease has begun to delineate molecular pathways underlying blood pressure variation, defining disease pathogenesis and identifying targets for therapeutic intervention. It is suggested that many genes have influences on the pathogenesis of hypertension (Lifton et al 2001;Gunes et al 2004;Bayramoglu et al 2012). This pathologic process is characterized by structural changes in the arterial wall caused by increased deposition of extracellular matrix (ECM) components, particularly collagen, as well as alterations in ECM architecture or cell-extracellular matrix attachments (Derosa et al 2006;Bayramoglu et al 2012).…”