Essential arterial hypertension (EAH) is a polygenic disease due to environmental, genetic, and epigenomic factors. The study aimed to establish the association of single nucleotide polymorphism (SNP) of AGTR1 (rs5186) and VDR (rs2228570) genes with the blood pressure (BP) elevation in EAH patients. 100 EAH subjects with hypertensive-mediated organ damaging (2nd stage), moderate, high, or very high cardiovascular risk were recruited into the case-control study. There were 70.83% females and 29.17% males, mean age 57.86±7.81 y.o. The control group included 60 healthy individuals of relevant age and gender distribution. Estimation of AGTR1 (rs5186) and VDR (rs2228570) gene polymorphism was performed by Real-Time Polymerase Chain Reaction. In EAH patients, the AGTR1 gene (rs5186) mutation occurs with a frequency of 2.78% in the absence of such among healthy individuals. The VDR (rs2228570) gene mutation occurs with a frequency of 23% cases. The C-allele carriers’ (AGTR1 gene) numbers with 2nd and 3rd BP values degree dominate over AA-genotype patients by 25.32% (χ2=4.52; р=0.033). VDR gene (rs2228570) polymorphic variants do not link to BP elevation values. Thus, the C-allele of the AGTR1 gene (rs5186) is associated with BP elevation in hypertensive patients. BP values do not depend on VDR gene (rs2228570) polymorphic variants.
Objective: The aim of the study was to analyze metabolic and hormonal parameters changes in patients with essential arterial hypertension (EAH) depending on the vitamin D receptor gene (VDR, rs2228570) polymorphism. Design and method: The study involved 100 patients suffering from EAH with target-organ damaging, moderate, high or very high cardiovascular risk. Among them were 79.0% (79) women and 21.0% (21) men, an average age was 59.87±8.02 yo. The control group involved 60 practically healthy persons, matched by age and gender distribution. All enrolled/screened patients signed the Informed Consent to participate in the research. The VDR gene (rs2228570) polymorphism was studied by a real-time polymerase chain reaction (RT-PCR) method. The intact parathyroid hormone (intact PTH) and vitamin 25 (OH) D levels in blood serum were determined by chemiluminescence immunoassay (MAGLUMI). Results: The decreased level of vitamin 25 (OH) D (<30 ng/ml) was found more often in the A-allele carriers of the VDR gene (rs2228570), than in GG-genotype carriers: in the control group - by 36.84% (x2 = 10.32; p = 0.001), in study group - by 42.42% (x2 = 39.27; p<0.001). Hypocalcemia according to the level of ionized blood calcium (Ca2+ <1.12 mmol/l) was registered only in G-allele carriers, both among practically healthy and hypertensive patients. In the control group, GG-genotype carriers had a lower ionized Ca2+ blood level with a compensatory higher concentration of the intact PTH in comparison with A-allele carriers - by 3.42%, 25.19% and 16.03% (p<0.05), respectively. Secondary hyperparathyroidism due to a compensatory increasing of the intact PTH (>65 pg/ml) was found more often in the G-allele carriers of the VDR gene (rs2228570) than in AA-genotype carriers: in control group - by 55.55% (x2 = 11.11; p<0.001), and in the group of patients with EAH - by 62.5% (x2 = 12.5; p<0.001). Conclusions: The GG-genotype of the VDR gene (rs2228570) increases the risk of hypocalcemia by more than 6 times [OR = 6.25; 95% CI: 1.05-37.37; p = 0.046], with the lowest probability in carriers of the A-allele [OR = 0.16; 95% CI: 0.03-0.96].
Objective:Endothelial nitric oxide synthase (eNOS) gene meet the criteria for candidate genes of cardiovascular disease, including essential arterial hypertension (EAH). The aim of the study was to evaluate the association of eNOS gene polymorphism (894G>T, 786T>C) with EAH risk, lipids profile and some concomitant diseases.Design and method:100 EAH patients with target-organ damage, moderate, high/very high cardiovascular risk were involved in the case-control study. 79.0% females and 21.0% males, mean age 59.87 ± 8.02; disease duration 6–25 years. Control included 48 practically healthy persons of relevant age. eNOS gene polymorphisms (894G>T, 786T>C) was examined by Real-Time PCR. Lipids’ profile was studied by total cholesterol (TC), high-, low density cholesterol (HDL-C, LDL-C), triglycerides (TG) and atherogenic index (AI).Results:eNOS gene mutants’ T-allele of 894G>T and C-allele of 786T>C were observed in 34.2% and 32.2% patients, that was almost 2 times less, than G-allele carriers (p = 0.006) and T-allele patients (p = 0.004) respectively. eNOS gene T-allele (894G>T) and C-allele (786T>C) were associated with increased relative risk of EAH 1.8 times [OR = 2.43; 95%CI:1.20–4.95] and 2.15 times [OR = 3.48; 95%CI:1.58–7.68], also with higher risk of concomitant Diabetes Mellitus type 2, cerebrovascular disease and acute myocardial infarction in anamnesis 1.53–1.72 times (p < 0.05). eNOS gene haplotype analysis proved the contribution of -894G/786C and -894T/786C haplotypes to EAH risk increase 2.05 times [OR95%CI:1.18–4.04] and 3.18 times [OR95%CI:1.27–7.29], elevation of TG level and atherogenic index by 10.5–18.7% (p < 0.05) and 12.65–14.19% (p < 0.05) accordingly. The HDL-C level was significantly lower in -894G/786C and -894T/786C carriers by 18.16% (p < 0.01) and 22.07% (p < 0.001). -894G/786T genotypes combination played a protective role against EAH [OR = 0.55; 95%CI:0.39–0.76; P < 0.001].Conclusions:eNOS gene -894G/786C and -894T/786C increased the EAH risk and lipids profile metabolism disorders.
Objective: Tight relationship between respiratory and vascular system appear obvious and several studies showed an association between lung function and hypertension. Furthermore, antihypertensive treatment itself might have an effect on lung function. Thus, the aim of this study was to determine association of hypertension and its treatment with respiratory function. Design and method: In order to evaluate the respiratory system functional state in hypertensive patients we studied 107 patients (mean 49,5±2,7 years old) with mild (1st group), moderate (2nd group) essential hypertension (EH) and neurocirculatory hypertensive asthenia (3d group), for control we observed 30 healthy subjects (4th group). Furthermore, stratification of treatment non-compliant and compliant patients was made to observe the possible impact of antihypertensive treatment. All patients had no chronic respiratory disease in anamnesis and were randomized dependently from the blood pressure levels. Parameters of the respiratory system function were examined by computer spirography. Results: Such predictive and active parameters of computer spirography as Maximum Voluntary Ventilation (MVV), Forced Vital Capacity (FVC), Forced Expiratory Volume after 1s (FEV1), FEV1 as % of Inspiratory Vital Capacity (FEV1%VCIN), FEV1 as % of FVC (FEV1E), and Peak Inspiratory Flow (PIF) did not significantly differ between 1st, 3d and 4th observed groups. But in the 1st and a little bit less in the 3d groups data of active parameters mentioned above were insignificantly lower (p>0.05) compared to healthy individuals. In the 2nd group patients MVV, FEV1%VCIN, FEV1E were uncertainly lower (p>0.05) than in the 1st and 3d groups, but were still border-normal with tendency to forming combined respiratory and heart failure. Antihypertensive treatment was associated with a deterioration in FEV1 by -150.3±12.78 ml (p = 0.01) and in FVC by -190.2±20.05 ml (p<0.01). With both high blood pressure and antihypertensive medication as individual variables in one regression model, only medication decreased FEV1 and FVC statistically significantly (p<0.01). Conclusions: Thus, a tendency for aggravation of the active parameters of respiratory function in patients with arterial hypertension is dependent on the blood pressure levels and use of antihypertensive medications.
Objective:Renin-angiotensin aldosterone system plays a major role in blood pressure regulation. Aldosterone, synthesized in the adrenal cortex by aldosterone synthase is encoded by the cytochrome 11B2 aldosterone synthase gene (CYP11B2). The aim of the study was to analyze the association of aldosterone synthase gene (CYP11B2) biallelic polymorphism (-344C/T) with Chronic Kidney Disease (CKD) in patients with essential arterial hypertension (EAH) in West-Ukrainian population.Design and method:One-hundred subjects with EAH and target-organ damaging (2nd stage), moderate, high or very high cardiovascular risk were involved in the case-control study. Among them 79.0% (79) females and 21.0% (21) males, mean age 59.87 ± 8.02 yo; disease duration from 6 to 25 years. CKD was determined by the National Kidney Foundation recommendations (Kidney Disease: Improving Global Outcomes (KDIGO), 2012) after glomerular filtration rate (GFR) decline < 60 ml/min/1.73sq.m for over 3 months (by Cockroft-Gault formula and CKD-EPI for Cystatin-C and Creatinine serum levels depending on gender). CKD was diagnosed in 29 persons. All enrolled / screened patients signed the Informed Consent to participate in the research. Control group included 48 practically healthy persons of relevant age. Gene polymorphism of aldosterone synthase gene CYP11B2 (-344C/T) was examined by polymerase chain reaction (PCR).Results:The probability of EAH in observed population increased 1.49 times in T-allele carriers of CYP11B2 gene, but only in females [OR = 1.90; 95%CI:1.02–3.54; p = 0.029], with contrary decreasing in C-allele women (p = 0.041). No relevant dependences were observed in hypertensive males. Also T-allele increased probability of CKD (GFR< 60 ml/min/1,73m2) in hypertensive population 1.48 times [OR = 1.86; 95%CI:1.01–3.58; p = 0.049], especially in T-allele females 1.53 times [OR = 6.51; 95%CI:1.39–30.60; p = 0.007] with low CKD risk in T-allele males [OR = 0.15; 95%CI:0.03–0.72; p = 0.009], respectively. Some predictors like DM2, the 2nd and 3rd grades of Obesity, and the 3rd grade level of Blood Pressure elevation escalated the risk of CKD 2.4, 2.08–2.32 and 2.91 times, accordingly (p< 0.05).Conclusions:Aldosterone synthase gene CYP11B2 (-344C/T) is associated with EAH. T-allele increased risk of CKD in hypertensive population, especially in females.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.