Development Of Essential Hypertension Research Articles

Clinical and genetic analysis of essential hypertension with mitochondrial tRNAMet 4435A>G and YARS2 mutation.

To investigate the role of m.4435A>G and YARS2 c.572G>T (p.G191V) mutations in the development of essential hypertension. A hypertensive patient with m.4435A>G and YARS2 p.G191V mutations was identified from previously collected mitochondrial genome and exon sequencing data. Clinical data were collected, and a molecular genetic study was conducted in the proband and his family members. Peripheral venous blood was collected, and immortalized lymphocyte lines constructed. The mitochondrial transfer RNA (tRNA), mitochondrial protein, adenosine triphosphate (ATP), mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) in the constructed lymphocyte cell lines were measured. Mitochondrial genome sequencing showed that all maternal members carried a highly conserved m.4435A>G mutation. The m.4435A>G mutation might affect the secondary structure and folding free energy of mitochondrial tRNA and change its stability, which may influence the anticodon ring structure. Compared with the control group, the cell lines carrying m.4435A>G and YARS2 p.G191V mutations had decreased mitochondrial tRNA homeostasis, mitochondrial protein expression, ATP production and MMP levels, as well as increased ROS levels (all P<0.05). The YARS2 p.G191V mutation aggravates the changes in mitochondrial translation and mitochondrial function caused by m.4435A>G through affecting the steady-state level of mitochondrial tRNA and further leads to cell dysfunction, indicating that YARS2 p.G191V and m.4435A>G mutations have a synergistic effect in this family and jointly participate in the occurrence and development of essential hypertension.

Primary Role of the Kidney in Pathogenesis of Hypertension.

Previous transplantation studies and the concept of 'nephron underdosing' support the idea that the kidney plays a crucial role in the development of essential hypertension. This suggests that there are genetic factors in the kidney that can either elevate or decrease blood pressure. The kidney normally maintains arterial pressure within a narrow range by employing the mechanism of pressure-natriuresis. Hypertension is induced when the pressure-natriuresis mechanism fails due to both subtle and overt kidney abnormalities. The inheritance of hypertension is believed to be polygenic, and essential hypertension may result from a combination of genetic variants that code for renal tubular sodium transporters or proteins involved in regulatory pathways. The renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) are the major regulators of renal sodium reabsorption. Hyperactivity of either the RAAS or SNS leads to a rightward shift in the pressure-natriuresis curve. In other words, hypertension is induced when the activity of RAAS and SNS is not suppressed despite increased salt intake. Sodium overload, caused by increased intake and/or reduced renal excretion, not only leads to an expansion of plasma volume but also to an increase in systemic vascular resistance. Endothelial dysfunction is caused by an increased intracellular Na+ concentration, which inhibits endothelial nitric oxide (NO) synthase and reduces NO production. The stiffness of vascular smooth muscle cells is increased by the accumulation of intracellular Na+ and subsequent elevation of cytoplasmic Ca++ concentration. In contrast to the hemodynamic effects of osmotically active Na+, osmotically inactive Na+ stimulates immune cells and produces proinflammatory cytokines, which contribute to hypertension. When this occurs in the gut, the microbiota may become imbalanced, leading to intestinal inflammation and systemic hypertension. In conclusion, the primary cause of hypertension is sodium overload resulting from kidney dysregulation.

ASSOCIATION BETWEEN VITAMIN D LEVEL AND ESSENTIAL HYPERTENSION

Introduction: There is relationship between vitamin D deficiency and hypertension (HTN). The mechanism causing the development of HTN, the Renin Aldosterone Angiotensin System, was discovered to be strongly inhibited by vitamin D. This study was piloted to assess the role of vitamin D deficiency in the development of essential hypertension (EH). Methods: A total of 50 patients with EH and 50 healthy participants participated in this study. Every participant was subjected to clinical history, physical examination, and other necessary blood testing, electrocardiography, and echocardiography. Results: There was a significant decrease in vitamin D in hypertensive group (20.25±3.28 ng/mL) than normotensive group (38.33±6.89 ng/mL). Vitamin D level was moderately negative correlated with systolic blood pressure (BP) (r – 0.43, p – 0.001), strong negative correlation with diastolic BP (r – 0.76, p&lt;0.001), strong negative correlation with intimal thickness (r – 0.67, p&lt;0.001), and moderate negative correlation with ventricular mass (r – 0.48, p&lt;0.001). Intimal thickness and ventricular mass were significantly higher in patients with EH with low vitamin D than those with normal vitamin D levels. Conclusion: There is a strong inverse relationship between serum vitamin D and HTN. Vitamin D deficiency levels are considered an additional risk factor for cardiovascular morbidity and mortality.

Pathophysiology of primary hypertension in children and adolescents.

The progress in research on the physiology of the cardiovascular system made in the last 100years allowed for the development of the pathogenesis not only of secondary forms of hypertension but also of primary hypertension. The main determinants of blood pressure are described by the relationship between stroke volume, heart rate, peripheral resistance, and arterial stiffness. The theories developed by Guyton and Folkow describe the importance of the volume factor and total peripheral resistance. However, none of them fully presents the pathogenesis of essential hypertension. The multifactorial model of primary hypertension pathogenesis developed by Irving Page in the 1940s, called Page's mosaic, covers most of the pathophysiological phenomena observed in essential hypertension. The most important pathophysiological phenomena included in Page's mosaic form a network of interconnected "nodes". New discoveries both from experimental and clinical studies made in recent decades have allowed the original Page mosaic to be modified and the addition of new pathophysiological nodes. Most of the clinical studies confirming the validity of the multifactorial pathogenesis of primary hypertension concern adults. However, hypertension develops in childhood and is even perinatally programmed. Therefore, the next nodes in Page's mosaic should be age and perinatal factors. This article presents data from pediatric clinical trials describing the most important pathophysiological processes associated with the development of essential hypertension in children and adolescents.

Clinical and genetic analysis of essential hypertension with CYB gene m.15024G>A mutation.

To explore the role of mitochondrial CYB 15024G>A mutation in the development of essential hypertension. Mitochondrial genome sequences of hypertensive patients were obtained from previous studies. Clinical and genetic data of a hypertensive patient with mitochondrial CYB 15024G>A mutation and its pedigree were analyzed. Lymphocytes derived from patient and family members were transformed into immortalized lymphoblastoid cell lines, and the levels of adenosine triphosphate (ATP), mitochondrial membrane potential and intracellular reactive oxygen species (ROS) were detected. The penetrance of this essential hypertension family was 42.9%, and the age of onset was 46-68 years old. Mitochondrial genome sequencing results showed that all maternal members carried a highly conserved mitochondrial CYB 15024G>A mutation. This mutation could affect the free energy of mitochondrial CYB for secondary and tertiary structure and protein folding, thereby changing its structural stability and the structure of the electron transfer function area around the mutation site. Compared with the control, the cell line carrying the mitochondrial CYB 15024G>A mutation showed significantly decreased levels of mitochondrial CYB, ATP and mitochondrial membrane potential, and increased levels of ROS (P<0.01). Mitochondrial CYB 15024G>A mutation may affect the structure of respiratory chain subunits and mitochondrial function, leading to cell dysfunction, which suggests that the mutation may play a synergistic role in essential hypertension.

Bioinformatics analysis of lncRNA-related ceRNA networks in the peripheral blood lymphocytes of Kazakh patients with essential hypertension in Xinjiang.

Here, we aimed to investigate long non-coding RNA (lncRNA) expression characteristics in the peripheral blood lymphocytes of Xinjiang Kazakh people with essential hypertension and the underlying regulatory mechanisms of competing endogenous RNAs (ceRNA). From April 2016 to May 2019, six Kazakh patients with essential hypertension and six Kazakh healthy participants were randomly selected from the inpatient and outpatient cardiology departments of the First Affiliated Hospital of Shihezi University Medical College, Xinjiang. After detecting the expression levels of lncRNA and mRNA in the peripheral blood lymphocytes using gene chip technology, their levels in the hypertensive group were compared with those in the control group. Six differentially expressed lncRNAs were randomly selected for real-time PCR to verify the accuracy and reliability of the gene chip results. GO functional clustering and KEGG pathway analyses were performed for differentially expressed genes. The ceRNA regulatory network of lncRNA-miRNA-mRNA was constructed, followed by visualization of the results. The expressions of miR-139-5p and DCBLD2 after PVT1 overexpression in 293T cells were detected by qRT-PCR and Western blot. In the test group, 396 and 511 differentially expressed lncRNAs and mRNAs, respectively, were screened out. The trend of real-time PCR results was consistent with that of the microarray results. The differentially expressed mRNAs were found to be primarily involved in the adhesion spot, leukocyte migration via endothelial cells, gap junction, actin cytoskeleton regulation, and extracellular matrix-receptor interaction signaling pathways. By constructing the ceRNA regulatory network, we found that lncRNA PVT1-miR-139-5p-DCBLD2 has a potential ceRNA regulatory mechanism involved in the development of essential hypertension in Xinjiang Kazakh people. In 293T cells, lncRNA PVT1 overexpression inhibited miR-139-5p and DCBLD2 levels. Our findings indicate that differentially expressed lncRNAs may be involved in the development of essential hypertension. lncRNA PVT1-miR-139-5p-DCBLD2 was indicated to comprise a potential ceRNA regulatory mechanism involved in the development of essential hypertension in the Xinjiang Kazakh population. Thus, it may act as a novel screening marker or therapeutic target for essential hypertension in this population.

CircHIPK2 facilitates phenotypic switching of vascular smooth muscle cells in hypertension.

Hypertension is a clinical syndrome characterized by increased systemic arterial blood pressure, affecting about 1.4 billion people currently worldwide with only one in seven cases adequately controlled. It is the main contributing factor of cardiovascular diseases (CVDs), often co-existing with other CVDs risk factors to impair the structure and function of important organs such as heart, brain, and kidney, and ultimately lead to multi-organ failure. Vascular remodeling is a critical process in the development of essential hypertension, and phenotype switching of vascular smooth muscle cells (VSMCs) was reported contributing substantially to vascular remodeling. circHIPK2 is a circular RNA (circRNA) derived from the second exon of homeodomain-interacting protein kinase 2 (HIPK2). Several studies revealed that circHIPK2 functions in various diseases by serving as a microRNA (miRNA) sponge. However, the functional roles and molecular mechanisms of circHIPK2 in VSMC phenotype switching and hypertension are not clear. In the present study, we showed that the expression of circHIPK2 was significantly upregulated in the VSMCs of hypertensive patients. Functional studies showed that circHIPK2 promoted the Angiotensin II (AngII)-induced VSMC phenotype switching by acting as the sponge of miR-145-5p, thereby upregulating the expression of a disintegrin and metalloprotease (ADAM) 17. Collectively, our study provides a new therapeutic target for hypertension.

Homoeopathic management of stress of essential hypertension patients : A literature review

Hypertension kills insidiously as it is commonly asymptomatic. Stress is conceived to be a significant contributing element towards development of essential hypertension. Homeopathy being the second largest system of medicine has immense scope, allowing in depth study of stress and offering individualized approach to these cases of stress led essential hypertension. There are several homoeopathic medicines which could prove useful in managing stress of essentialhypertension. This article attempts to review some of the existing literature in this context discussing role of homoeopathy in management of stress of essential hypertension patients.

Hypertension in peri- and postmenopausal women — pathophysiological mechanisms and approaches to treatment

This review presents epidemiological data on the effect of sex hormones and reproductive status on the level of blood pressure (BP) and the incidence of es­sential hypertension (EHT) in women. The role of estrogen deprivation and hyper­androgenism in the development of EHT in peri- and postmenopause is discussed. The main mechanisms of EHT in periand postmenopausal women: sympathetic and renin-angiotensin-aldosterone system hyperactivity, salt-sensitivity, high prevalence of abdominal obesity, metabolic syndrome, left ventricular hypertrophy, left atrial dilatation and high risk of atrial fibrillation, stroke and heart failure with preserved left ventricle ejection fraction. Data on the efficacy and tolerability of the main classes of antihypertensive drugs in women is presented. We discussed the mechanisms of selective I1-imidazoline receptor agonists and the results of cohort studies of moxonidine monotherapy and its combination with other antihypertensive drugs and hormonal menopausal therapy in peri- and post­menopausal women. Moxonidine reduces high blood pressure in peri- and postmenopausal women and has a beneficial effect on metabolic syndrome components, but is also effective in patients with hypertensive crises, especially with sympathetic hyperactivity.

Effects of potassium channel knockdown on peripheral blood T lymphocytes and NFAT signaling pathway in Xinjiang Kazak patients with hypertension

ABSTRACT Backgroud and aim T lymphocytes are involved in the occurrence and development of essential hypertension, and potassium channels are thought to be critical for lymphocyte activation. This study is to examine the roles of the voltage-gated potassium channels (Kv1.3) and calcium-activated potassium channels (KCa3.1) in peripheral blood T lymphocytes in Kazakh hypertensive patients of Xinjiang, China, mainly focusing on the effects of these channels on nuclear factor of activated T cells (NFAT) and inflammatory cytokines of T lymphocytes. Method Kv1.3 and KCa3.1 gene silencing were performed in cultured T lymphocytes from Kazakh patients with severe hypertension. T cell proliferation after gene silencing was measured using CCK-8. The mRNA and protein expression levels were measured using RT-qPCR and Western blot analysis, respectively. Nuclear translocation of NFAT was observed using laser confocal fluorescence microscopy. Inflammatory cytokine levels were detected with ELISA. Results Compared with control group, gene silencing of Kv1.3 and KCa3.1 respectively inhibited the proliferation of T cells. Moreover, compared with the control group, the mRNA expression levels of NFAT, IL-6 and IFN-γ were significantly decreased after gene silencing. Furthermore, the NFAT protein expression level was significantly down-regulated. In addition, the levels of IFN-γ and IL-6 in the cell culture supernatant were significantly decreased. Conclusion Both Kv1.3 and KCa3.1 potassium channels activated T lymphocytes and enhanced the cytokine secretion possibly through CaN/NFAT signaling pathway, which may in turn induce micro-inflammatory responses and trigger the occurrence and progression of hypertension.

Relationship of Toll-Like Receptors 2 and 4 Gene Polymorphisms with Essential Hypertension in Chinese Han Population

Objective: There are numerous studies suggesting that genetic polymor-phisms of inflammation factors Toll-like receptors 2 and 4 (TLR2, TLR4) might play a role in the pathophysiological process of hypertension. In this study, we evaluated the association in a sample of members of the Chinese Han population. Method: We selected four single nucleotide polymor-phisms (SNP) of TLR2 (rs3804099, rs3804100, rs7656411) and TLR4 (rs1927906) genes, and measured the distributions of genotypic and allelic frequencies in 1063 participants, including 391 essential hypertension pa-tients and 672 controls. Result: No significant differences in the genotypic and allelic frequencies of the four SNPs were detected between cases and controls. However, three haplotypes, CCG, TTG and TTT of TLR2, were significantly associated with a decrease in the risk of essential hyperten-sion (OR: 0.512, 95% CI: 0.397 - 0.660, P P = 0.0038; OR: 0.797, 95% CI: 0.667 - 0.952, P = 0.0122, respectively). Inversely, the risk of essential hypertension increased sig-nificantly in patients with the CTG, TCG or TCT haplotypes (OR: 2.924, 95% CI: 2.157 - 3.963, P P P TLR2 might have profound effects on the development of essential hypertension in the Chinese Han population.

Extracellular Vesicles and Hypertension.

Hypertension implicates multiple organs and systems, accounting for the majority of cardiovascular diseases and cardiac death worldwide. Extracellular vesicles derived from various types of cells could transfer a variety of substances such as proteins, lipids, and nucleic acids from cells to cells, playing essential roles in both physiological and pathological processes. Extracellular vesicles are demonstrated to be closely associated with the development of essential hypertension by mediating the renin-angiotensin-aldosterone system and crosstalk between multiple vascular cells. Extracellular vesicles also participate in various kinds of pathogenesis of secondary hypertensions including acute kidney injury, renal parenchymal diseases, kidney transplantation, secretory diseases (primary aldosteronism, pheochromocytoma and paraganglioma, Cushing's syndrome), and obstructive sleep apnea. Extracellular vesicles have been proved to have the potential to be served as new biomarkers in the diagnosis, treatment, and prognosis assessment of hypertension. In the future, large multicenter cohorts are highly in demand for further verifying the sensitivity and specificity of extracellular vesicles as biomarkers.

The role of polymorphism of AGT genes (rs4762) and GNB3 (rs5443) in the development of essential hypertension

Assess the role of the polymorphism of AGT genes (rs4762) and GNB3 genes (rs5443) in the development of the essential arterial hypertension separately and by combining their polymorphic variants.Material and methods. The case-control study involved 100 patients with EAH stage II, 1-3 degrees of blood pressure (BP), high and very high cardiovascular risk. Among the patients, 21% (21) constituted men, and 79%(79) were women. The mean age of patients was 59.86±6.22 y.o. The control group comprised 60 almost healthy individuals, relevant in age (49.13±6.28y.o.) and gender distribution (63% - women, 37% - men). To study of polymorphism of AGT (rs4762) and GNB3 (rs5443) genes, we performed a qualitative polymerase chain reaction (PCR) in real time.Results. In patients with EAG residents of Northern Bukovyna mutated T-allele of AGT gene (rs4762) is found in 15,97% of cases, which is more frequent than in practically healthy by 9,72% (p=0,023); mutations of AGT gene in homozygous species in the control group have not met at all. Binary logistic regression confirmed an increase in the risk of inheriting EAH according to dominant and additive models in carriers of the minor T-allele of the AGT gene (rs4762) almost 3 times higher than in homozygotes for the major C-allele (р=0,04 і р=0,03). Inheritance of EAH is not associated with polymorphic variants of the GNB3 gene (rs5443).&#x0D; Conclusions. Тhe T-allele of the AGT gene (rs4762) increases the risk of development of EAH almost 3 times, while the polymorphic variants of the GNB3 gene (rs5443) are not the predictors of the emergence of EAH in the population.

Role of Nutritional and Environmental Factors in the Development of Essential Hypertension among School-going Adolescents in Chennai, Tamil Nadu.

Background:Essential hypertension is one of the fastest rising noncommunicable diseases among adolescents and poses a major public health issue globally. This study aimed to estimate the prevalence of prehypertension and hypertension among school-going adolescents in Chennai and also to delineate the role of nutritional and environmental determinants in the development of hypertension.Methods:This cross-sectional study was conducted among school-going adolescents aged 14 to 18 years in northern Chennai. Four schools (two private, two public) out of 21 were selected randomly using probability proportionate to sampling size and 401 students were recruited after consent. Data were collected using an adapted modified World Health Organization (WHO) Global School-based student Health Survey (GSHS) questionnaire; anthropometry and blood pressure measurements were done by trained healthcare professionals using standard procedures. Prehypertension was defined when systolic or diastolic pressure >90th percentile and <95th percentile; hypertension when systolic or diastolic pressure >95th percentile. Data were analyzed using SPSS, descriptive statistics like frequencies, mean, and percentages were used and inferential statistics like Chi-square test and logistic regression were used to elicit predictors of essential hypertension.Results:Out of 401 participants, 185 (46.1%) were males and 216 (53.9%) were females. Overall prevalence of prehypertension and hypertension was 14.2% and 5.5%, respectively. Gender (P = 0.039), overweight/obese (P = 0.000), junk food intake for >3 days/week (P = 0.000), physical inactivity for <3 days/week (P = 0.000), and parent's history (P = 0.005) were significant determinants in the development of prehypertension and hypertension.Conclusions:Nutritional and environmental determinants play a critical role in influencing blood pressure status among adolescents, this requires lifestyle and behavioral modification.

The Role of Urotensin-II in Obesity and Metabolic Syndrome in Pediatric Population.

Background: Urotensin-II (U-II) is a short cyclic peptide that is widely recognized as one of the most potent vasoconstrictors. U-II plays a role in the pathophysiology of MS, participating in the development of essential hypertension, insulin resistance, hyperglycemia, and a proinflammatory state. Methods: This study comprised 52 obese children and adolescents with a body mass index (BMI) z score > 2, aged 10 to 18 years. Serum levels of U-II were assessed using an enzyme-linked immunosorbent assay along with other standard biochemical parameters. Results: Elevated serum levels of U-II were recorded in the group of obese subjects with MS when compared with the group of obese subjects without MS (4.99 (8.97–3.16) vs. 4.17 (5.17–2.03) ng/mL, median and IQR, p = 0.026). Furthermore, a subgroup of study subjects with high blood pressure had significantly higher U-II levels in comparison with the normotensive subgroup (4.98 (7.19–3.22) vs. 3.32 (5.06–1.97) ng/mL, p = 0.027), while the subgroup with a positive family history of high blood pressure had significantly higher U-II levels when compared with subjects who had a negative family history of elevated blood pressure (5.06 (6.83–4.45) vs. 3.32 (6.13–2.21) ng/mL, p = 0.039). Conclusions: To the best of the author’s knowledge, this is the first study on the levels of U-II in obese children and adolescents, including a possible link to MS.

MTHFR C677T (rs1801133) genetic polymorphism is associated with development risk of essential hypertension in the Turkish population

BackgroundHypertension is a serious condition that is spread worldwide and may lead to severe complications such as heart attack, stroke, hypertensive retinopathy, and renal failure. Although some genetic and environmental risk factors are known to play a role in the etiology of hypertension, like most of the other multi-factorial diseases, its etiology is yet to be fully elucidated. Our study aimed to investigate the effects of methylenetetrahydrofolate reductase (MTHFR) C677T (rs1801133) and A1298C (rs1801131), factor V Leiden (FVL) G1691A (rs6025), and prothrombin (PT) G20210A (rs1799963) genetic polymorphisms on the development risk of essential hypertension and level of blood pressure in hypertensive patients.ResultsThe frequency of the homozygous polymorphic TT genotype for the MTHFR C677T polymorphism was significantly higher in male hypertensive patients than in the male control group (27% vs 6.3%, p = 0.028). The rate of the variant T allele for the MTHFR C677T polymorphism was also significantly higher in male hypertensive patients compared to male healthy controls (51.4% vs 21.9%, p = 0.0004). There was no difference among hypertensive patients and healthy controls regarding the frequencies of MTHFR A1298C, FVL G1691A and PT G20210A polymorphisms. In addition, we found no difference between genotype groups regarding systolic and diastolic blood pressure levels in hypertensive patients.ConclusionsHomozygous polymorphic TT genotype and variant T allele for the MTHFR C677T polymorphism may be considered as a risk factor for the development of essential hypertension in the Turkish male population.

Neurophysiological justification of the G. F. Lang hypothesis about the occurrence of essential hypertension

This article is an analysis of modern data on the morphological, functional and neurochemical organization of the central mechanisms of blood circulation regulation, the violation of which can cause the development of essential hypertension. The data indicating the validity of the hypothesis of G.F. Lang that prolonged emotional stress leads to a violation of the neuronal activity of the hypothalamus structures are presented. The article describes the morphological connections of the hypothalamus with the neurons of the ventrolateral region of the medulla oblongata and the structures of the spinal cord that provide neurogenic vascular tone. The evidence of convergence of axons of neurons of the paraventricular nucleus of the hypothalamus on the preganglionic neurons of the spinal cord is presented. Neurochemical processes in the vasomotor center of the medulla oblongata are considered, morphological changes of preganglionic sympathetic neurons in experimental arterial hypertension are indicated.

A Study on Serum Nitric Oxide and Hydrogen Sulfide in Essential Hypertension Cases in a Tertiary Care Hospital in West Bengal

Background-Essential hypertension is a multifactorial disease of unknown etiology characterized by a chronic elevation of blood pressure without any secondary causes. Nitric oxide and hydrogen sulfide are vasodilatory gasotransmitters whose deficiency results in endothelial dysfunction and vasoconstriction and hence is one of the etiological factors in the development of hypertension. Aims and Objectives – The study aimed to estimate the serum levels of NO and H₂S and to find out their correlation in essential hypertension cases and normotensive controls. Materials and Methods- Serum levels of NO and H₂S were measured using chemical methods, in fifty patients with essential hypertension and compared with fifty age-matched controls. Results- The mean serum NOx level in essential hypertension cases is 45.45 ± 11.09 µmol/L which is significantly lower (p-value &lt;0.001) than that of controls where it is 166.40 ± 16.63 µmol / L. The mean serum H₂S level in essential hypertension cases is 45.61 ± 11.01 µmol/ L which is again significantly lower ( p-value &lt;0.001) than controls in which it is 111.54 ± 9.60 µmol/ L. A statistically significant positive correlation exists between serum NOx and H₂S levels in overall study subjects. Conclusion- This study demonstrates that both the serum levels of NO and H₂S decrease with an increase in BP in essential hypertension cases. There exists a positive correlation between NO and H₂S in overall study subjects. Thus, the simultaneous decline in bioavailability of both NO and H₂S is a significant underlying cause in the development of essential hypertension.

Sleep disorders — risk factors and hypertension markers in young people with normal body weight

Aim. To assess the relationship between different types of sleep disorders, sleep-related symptoms and hypertension (HTN).Material and methods. This cross-sectional study based on the online survey of persons aged 18-39 years with a body mass index of 18-25 kg/m2.Results. According to the results, the HTN risk in persons aged 18-39 years with normal body mass index increases 2 or more times in the presence of various types of sleep disorders and related symptoms. The prevalence of HTGN depends on the patient's phenotype, i.e. from a combination of different types of sleep disorders and sleep-related symptoms.Conclusion. Given the widespread prevalence of various sleep disorders, as well as the relationship between sleep disorders and hypertension in young people, it is necessary to develop preventive measures aimed at reducing the HTN risk by restoring healthy sleep. We also suggest that various sleep disorders may be the primary link in the development of essential HTN.

Prevention of Hypertension at Home

Hypertension is a systolic blood pressure (SBP) value of 130mmHg or more and / or a diastolic blood pressure (DBP) of more than 80 mmHg. One of the factors in the development of essential hypertension is the patient's genetic ability to respond to salt. Various non-pharmacological interventions have been shown to be effective in lowering blood pressure and preventing hypertension. The most effective interventions are weight loss, reduced Na + intake, increased potassium intake, increased physical activity, reduced alcohol consumption and a diet such as Diet Approaches to Stop Hypertension (DASH) which combines several elements that are useful in controlling blood pressure. A diet that emphasized fruit and vegetable intake significantly reduced high blood pressure during the 8-week intervention. Some things we can do to help reduce hypertension at home are to maintain a diet and daily lifestyle and can be done through hydrotherapy (soaking your feet in warm water).