Cause Of Essential Hypertension Research Articles

Sensitization of Hypertension: The Impact of Earlier Life Challenges: Excellence Award for Hypertension Research 2021.

Hypertension affects over 1 billion individuals worldwide. Because the cause of hypertension is known only in a small fraction of patients, most individuals with high blood pressure are diagnosed as having essential hypertension. Elevated sympathetic nervous system activity has been identified in a large portion of hypertensive patients. However, the root cause for this sympathetic overdrive is unknown. A more complete understanding of the breadth of the functional capabilities of the sympathetic nervous system may lead to new insights into the cause of essential hypertension. By employing a unique experimental paradigm, we have recently discovered that the neural network controlling sympathetic drive is more reactive after rats are exposed to mild challenges (stressors) and that the hypertensive response can be sensitized (ie, hypertensive response sensitization [HTRS]). We have also found that the induction of HTRS involves plasticity in the neural network controlling sympathetic drive. The induction and maintenance of the latent HTRS state also require the functional integrity of the brain renin-angiotensin-aldosterone system and the presence of several central inflammatory factors. In this review, we will discuss the induction and expression of HTRS in adult animals and in the progeny of mothers with prenatal obesity/overnutrition or with maternal gestational hypertension. Also, interventions that reverse the effects of stressor-induced HTRS will be reviewed. Understanding the mechanisms underlying HTRS and identifying the beneficial effects of maternal or offspring early-life interventions that prevent or reverse the sensitized state can provide insights into therapeutic strategies for interrupting the vicious cycle of transgenerational hypertension.

EHypertension: A prospective longitudinal multi‐omics essential hypertension cohort

eHypertension: A prospective longitudinal multi‐omics essential hypertension cohort

Assessment of Cholesteryl Ester Transfer Protein Gene Taq1B Polymorphism and Its Relationship with Lipid Levels of Hypertensive Iraqi Patients

Lipid disorder is one of the main causes of essential hypertension. Cholesteryl ester transfer protein (CETP) gene polymorphism is known to be associated with changes in lipid profile. Therefore, this study designed to detect the CETP Taq1 B polymorphism (rs708272) and evaluate its relationship with lipid profile levels among some hypertensive Iraqi patients. One hundred and seventy blood samples were collected from two groups, the first group included a hundred hypertensive patients and the second group included seventy healthy individuals as control group. For both groups, lipid profile was estimated, genomic DNA was extracted from all samples and Polymerase Chain Reaction - Restriction Fragment Length Polymorphism (PCR-RFLP) technique was used to detect CETP gene Taq1 B polymorphism. Results indicated that levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL-C), and very-low-density lipoprotein (VLDL-C) had increased, while the level of high-density lipoprotein (HDL-C) was decreased in hypertensive patients in comparison to control group. The study also showed that the frequency of B1B1 genotype and (B1) allele was higher in hypertensive patients in compare with control group (p ≤ 0.01). Lipid profile concentrations according to CETP gene Taq1 B genotypes showed non-significant differences. This study concluded that the CETP gene Taq1B polymorphism may associated with associated with lipid disorder and CETP (B1) allele which could be used as a genetic marker for increasing hypertensive susceptibility in Iraqi population.

Serum calcium levels in newly detected essential hypertensive patients

Background: Systemic hypertension is global disease responsible for significant mortality and morbidity. Essential or primary hypertension accounts for the majority of people with hypertension. Although our understanding of the pathophysiology of essential hypertension has grown a lot, its aetiology still remains hypothetical. Few studies in literature have found some correlation with serum calcium levels and blood pressure of the individuals.Methods: A total 200 patients, 100 newly diagnosed essential hypertensive and 100 normotensive patients were included in the study. A detailed history and clinical profile was taken. Blood sample was collected and serum calcium, serum albumin were determined and corrected calcium was calculated and the results were tabulated and appropriate statistical analysis was done.Results: The mean total serum calcium and corrected calcium levels were significantly lowered in essential hypertensive compared to the normotensive individuals. There was no correlation between total serum and corrected calcium levels against systolic and diastolic blood pressure. There was also no difference in serum total and corrected calcium levels among different subsets in essential hypertensive group.Conclusion: Essential hypertension still remains the most common form of hypertension present worldwide causing significant mortality and morbidity. Despite increased advances in medicine and large number of studies done in context with the cause of essential hypertension, its aetiology still remains hypothetical. Even though studies have shown some correlation of calcium fractions with hypertension, the aetiology is still unclear.

Arteriosclerosis with superimposed atherosclerosis is the cause not the consequence of essential hypertension

The arterial system is a closed loop and the pressure within this loop reflects cardiac output, resistance to outflow, volume of fluid within the circulation and stiffness of the arterial wall. Increased resistance to outflow or Bayliss's phenomena cannot be the cause of essential hypertension as it reverses with treatment of hypertension. There is no evidence for increased cardiac output in essential hypertension. Increased blood volume contributes to hypertension in obesity just as it does in hypertension secondary to renal failure.The principle cause of essential hypertension is increasing stiffness of the arterial wall. This is a consequence of arteriosclerosis that commences in utero and progressively increases in severity with increasing age. Arteriosclerotic arterial wall stiffening antedates the onset of essential hypertension by decades. It not only explains the increasing incidence of essential hypertension with increasing age, but it is the only thing that fulfils Koch's first postulate and that is it is present in 100% of individuals with essential hypertension.

Up-regulation of circular RNA hsa_circ_0037909 promotes essential hypertension.

AimsEssential hypertension (EH) is a high prevalence disease facing a public health challenge. People were little known about the genetics of diagnosing the cause of EH. Circular RNAs that have a continuous cycle of covalent closure, without affected by RNA exonuclease, and are more stable and hard to degrade may involve into the molecule regulation mechanism of EH as an important biomedical.MethodsqRT‐PCR was used to analyze circRNAs in total volume of human blood and the induced human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). Our case‐control study was involved with 48 pairs of case controls with sex and age (±3 years) match. We conducted t test, Pearson's χ2 test, and receiver operating characteristics (ROC) curve analysis for the corresponding analysis.ResultsThe expression level of hsa_circ_0037909 in EH patients was significantly higher than that in the healthy controls (P = 0.007), and the expression level of hsa‐miR‐637 in EH patients was significantly lower in than that in the healthy controls (P = 0.039); the same result appears in the HAECs and HUVECs. Hsa‐miR‐637 (adjusted P = 0.018), hsa_circ_0037909 (adjusted P = 0.005), HDL (adjusted P = 0.024), and serum creatinine (adjusted P = 0.014) were brought into the model which performed logistic regression analysis. The combination of two RNAs was excellent (P < 0.001) through ROC curve analysis. Hsa_circ_0037909 was significantly positively correlated with serum creatinine (P < 0.001) and low‐density lipoprotein (LDL) (P = 0.017).ConclusionsOur findings suggested that the combination of hsa_circ_0037911 and hsa‐miR‐637 may be a significant important biomarker for early diagnosis of EH. Hsa_circ_0037909 may affect serum creatinine or LDL leading to the formation of EH.

Central nervous system neuroplasticity and the sensitization of hypertension.

The causes of essential hypertension remain an enigma. Interactions between genetic and external factors are generally recognized to act as aetiological mechanisms that trigger the pathogenesis of high blood pressure. However, the questions of which genes and factors are involved, and when and where such interactions occur, remain unresolved. Emerging evidence indicates that the hypertensive response to pressor stimuli, like many other physiological and behavioural adaptations, can become sensitized to particular stimuli. Studies in animal models show that, similarly to other response systems controlled by the brain, hypertensive response sensitization (HTRS) is mediated by neuroplasticity. The brain circuitry involved in HTRS controls the sympathetic nervous system. This Review outlines evidence supporting the phenomenon of HTRS and describes the range of physiological and psychosocial stressors that can produce a sensitized hypertensive state. Also discussed are the cellular and molecular changes in the brain neural network controlling sympathetic tone involved in long-term storage of information relating to stressors, which could serve to maintain a sensitized state. Finally, this Review concludes with a discussion of why a sensitized hypertensive response might previously have been beneficial and increased biological fitness under some environmental conditions and why today it has become a health-related liability.

Study of effects of yoga and pranayama on human reaction time and certain physiological parameters in normal and hypertensive subjects

Background: Yoga is a process of gaining control over the mind, as defined by Patanjali. Stress has been implicated as one of the major causes of essential hypertension. Yoga works on every cell of the body. Yoga influences body as well as controls the stress in the individual. An index of the processing ability of central nervous system and a simple means of determining sensory-motor performance is referred to as reaction time (RT). It has been proclaimed that human performance including central neural processing is improved by yoga training. It improves cardiorespiratory performance, balances autonomic nervous system, decreases pulse, respiratory rate, systolic and diastolic blood pressure. Aims and Objective: To show the effects of yoga and pranayam on auditory and visual RT and on certain physiological parameters such as weight, body mass index, pulse rate, respiratory rate, systolic blood pressure, and diastolic blood pressure in normal and hypertensive subjects. Materials and Methods: This comparative type of study included 70 normal and 70 hypertensive subjects. It was carried on subjects between 30 and 60 years of age. Auditory reaction time (ART) and visual reaction time (VRT) were studied in subjects with “Response Analyzer” reaction time apparatus. The physiological parameters such as weight, body mass index, pulse rate, respiratory rate, systolic blood pressure, and diastolic blood pressure were measured. Parameters were measured in two sittings; on admission to yoga center and after 3 months. Statistical software STATA Version 10.0 was used for statistical analysis. Result: It was found that changes in the RT and physiological parameters were significant in hypertensive subjects when compared with normal individuals. Conclusion: Yoga is a helpful intervention in hypertensive subjects. Yoga and pranayam are more beneficial to hypertensive subjects. RT is an index of cortical arousal, and a decrease in it indicates an improved sensory-motor performance and an enhanced processing ability of the central nervous system.

Interactions Between the Immune and the Renin-Angiotensin Systems in Hypertension.

The renin–angiotensin system (RAS) is an essential regulator of blood pressure homeostasis. The primary effector molecule of the RAS is angiotensin (Ang) II, an 8-amino acid peptide that initiates tissue-specific processes via binding to the type 1 or 2 angiotensin II receptors (AT1 or AT2). The AT1 receptor is a G-protein–coupled receptor expressed in most tissues throughout the body. Although the rodent expresses 2 AT1 receptor isoforms, AT1A and AT1B, the closest functional homolog to the human AT1 receptor in most rodent tissues is AT1A. The most widely appreciated functions of Ang II signaling via the AT1 receptor are to augment global vascular tone and to promote sodium retention in the kidney, thus playing a crucial role in acute and long-term maintenance of blood pressure.1,2 Ang II elicits these effects by increasing the contractility of vascular smooth muscle, promoting the release of aldosterone from the adrenal cortex, and directly increasing the expression or activity of solute transporters in the renal tubules that promote sodium reabsorption. As such, blockade of the RAS has been a mainstay in the treatment for hypertension and its complications, including cardiovascular and kidney disease.2,3 Although the cause of essential hypertension is unclear, inhibition of the RAS is effective in reducing blood pressure in a wide variety of patients, which suggests that inappropriate RAS activation is common in the pathogenesis of this idiopathic condition. Global RAS inhibitors ameliorate hypertension by blocking the production of Ang II or by preventing activation of the AT1 receptor. These medications are global inhibitors in the sense that they disrupt AT1 receptor signaling concomitantly in all tissues. The ongoing effort to uncover novel pathogenic mechanisms of hypertension has revealed a significant role for …

Association of cytomegalovirus infection with hypertension risk: a meta-analysis.

SummaryBackgroundInformation regarding association between cytomegalovirus (CMV) infection and essential hypertension (EH) risk is not consistent across studies. Therefore, we conducted a meta-analysis to investigate the association in detail.MethodsWe comprehensively searched the published literature from the PubMed and Embase databases for any study analyzing the association between CMV and EH risk. A random-effects model was used to calculate the pooled odds ratio (OR) with 95 % confidence interval (CI).ResultsThree studies involving 9657 patients were included in the meta-analysis, and the results showed a significantly increased risk of EH in patients with CMV infection. Overall, 79.3 % of the hypertension patients were CMV-positive, which was significantly higher than the percentage for controls (OR = 1.39, 95 % CI = 0.95–2.05, P = 0.017). There was significant heterogeneity among the studies included (I2 = 70.5 %). The funnel plot and Egger’s test also indicated no publication bias.ConclusionsThe results showed a significant association between CMV and EH, which indicates that CMV infection is a possible cause of EH.

Hypertension Impairs Cerebral Blood Flow in a Mouse Model for Alzheimer's Disease.

Hypertension, a risk factor for Alzheimer's disease (AD), is a treatable condition, which offers possibilities for prevention of AD. Elevated angiotensin II (AngII) is an important cause of essential hypertension. AngII has deleterious effects on endothelial function and cerebral blood flow (CBF), which may contribute to AD. AngII blocking agents can thus provide potential candidates to reduce AD risk factors in hypertensive patients. We studied the effect of 2 months induced hypertension (AngII-infusion via osmotic micropumps) on systolic blood pressure (SBP) and CBF in 10 months-old wild-type (WT) C57bl/6j and AβPPswe/PS1ΔE9 (AβPP/PS1) mice, and treatment with two different antihypertensives, 1) eprosartan mesylate (EM, 0.35mg/kg) or 2) hydrochlorotiazide (HCT, 7.5mg/kg), after 1 month of induced-hypertension. SBP was monitored twice each month via tail cuff plethysmography. CBF was measured with MR by flow-sensitive alternating inversion recovery. Chronic AngII-infusion induced an increase in SBP in both AβPP/PS1 and WT mice accompanied by a decrease in hippocampal and thalamic CBF only in the AβPP/PS1 mice. An additional difference between the AβPP/PS1 mice and WT mice was that SBP was much higher in AβPP/PS1 mice in both hypertensive and normotensive conditions. Moreover, both antihypertensives were less effective in reducing AngII-induced hypertension to normal levels in AβPP/PS1 mice, while being effective in WT mice. It can be concluded that AngII-induced elevated SBP results in impaired CBF and a decreased response to blood pressure lowering treatment in a transgenic model of AD. Our findings suggest a relation between midlife hypertension and decreased CBF in an AD mouse model, similar to the relation which has been found in AD patients. This translational mouse model could be used to investigate possible prevention and treatment strategies for AD.

Association between ins4436A in 11β-hydroxysteroid dehydrogenase type 1 gene and essential hypertension in Polish population.

Essential hypertension (EH) is the most common cardiovascular disease worldwide, and it has a strong genetic component. Cortisol homeostasis is an important factor in controlling blood pressure, and the availability of this hormone is regulated by 11βhydroxysteroid dehydrogenase type 1 enzyme (11βHSD1), which converts cortisone into cortisol. We investigated the correlation between EH and the single nucleotide polymorphism (SNP) ins4436A located on the hydroxysteroid (11-beta) dehydrogenase 1 gene among the Polish population. The study included a total of 268 patients with confirmed EH and 151 unrelated controls. All studied polymorphisms were detected using the restriction fragment length polymorphism (RFLP) method. The carriage of ins4436A (rs45487298) polymorphism in intron 3 of the HSD11B1 gene was more frequent among patients with EH than among controls (p=0.013). The analysis of association of ins4436A with the risk of EH indicated an odds ratio (OR) of 2.44 (95% confidential interval: 1.24-4.82). Moreover, essential hypertension occurred less frequently in males than in females. Results of multivariate analysis in the study group showed that ins4436A is a strong predictor of diabetes mellitus type 2 and ins4436A may lead to a decrease of the high-density lipoprotein (HDL) cholesterol level. The cause of essential hypertension has not been fully established, but genetic factors seem to play a very important role. In our study we found that ins4436A in the HSD11B1 gene was associated with essential hypertension in a Polish population. Nevertheless, the impact of ins4436A in the HSD11B1 gene on the occurrence of essential hypertension requires further investigations.

Plasma Metanephrines Are Associated With Glucose Metabolism in Patients With Essential Hypertension.

There is a high incidence of glucose intolerance in essential hypertension. Overactivation of the sympathetic system is one of important causes of essential hypertension. Whether sympathetic system affects glucose metabolism in patients with essential hypertension has never been reported previously. The aim of this study was to explore the association between the sympathetic system activity and glucose metabolism in patients with essential hypertension.A total of 202 essential hypertension inpatients without diabetes were recruited from Shanghai Ruijin Hospital between February 2006 and August 2013. Activity of sympathetic system was quantified by plasma metanephrines (MNs) levels. All subjects received an oral glucose tolerance test.Fasting plasma glucose and 2-hour plasma glucose increased significantly across the quartiles of plasma MNs. The multiple linear regression analysis revealed that plasma MNs were significantly associated with fasting plasma glucose and 2-hour plasma glucose. The area under curve of plasma glucose increased significantly from the lowest plasma MNs quartile across to the highest quartile. The multiple logistic regression analysis revealed that odds ratios (95% confidence interval) for prediabetes in the highest quartile compared with the lowest quartile of plasma MNs was 4.00 (95% confidence interval, 1.16–13.86).Plasma MNs levels are positively associated with plasma glucose in patients with essential hypertension. Patients with high plasma MNs levels had an increased risk of prediabetes.

The roles of sensitization and neuroplasticity in the long-term regulation of blood pressure and hypertension.

After decades of investigation, the causes of essential hypertension remain obscure. The contribution of the nervous system has been excluded by some on the basis that baroreceptor mechanisms maintain blood pressure only over the short term. However, this point of view ignores one of the most powerful contributions of the brain in maintaining biological fitness-specifically, the ability to promote adaptation of behavioral and physiological responses to cope with new challenges and maintain this new capacity through processes involving neuroplasticity. We present a body of recent findings demonstrating that prior, short-term challenges can induce persistent changes in the central nervous system to result in an enhanced blood pressure response to hypertension-eliciting stimuli. This sensitized hypertensinogenic state is maintained in the absence of the inducing stimuli, and it is accompanied by sustained upregulation of components of the brain renin-angiotensin-aldosterone system and other molecular changes recognized to be associated with central nervous system neuroplasticity. Although the heritability of hypertension is high, it is becoming increasingly clear that factors beyond just genes contribute to the etiology of this disease. Life experiences and attendant changes in cellular and molecular components in the neural network controlling sympathetic tone can enhance the hypertensive response to recurrent, sustained, or new stressors. Although the epigenetic mechanisms that allow the brain to be reprogrammed in the face of challenges to cardiovascular homeostasis can be adaptive, this capacity can also be maladaptive under conditions present in different evolutionary eras or ontogenetic periods.

4C.09

Objective: Hypertension is a risk factor for Alzheimer's disease (AD). It is a treatable condition which opens important avenues for prevention of AD. Elevated angiotensin II (AngII) is an important cause of essential hypertension and has deleterious effects on endothelial function and cerebral blood flow (CBF). In this study we therefore investigated the interaction between AngII, systolic blood pressure (SBP), and MRI-measurements in the APPswe/PS1[Delta]E9 (APP/PS1) mouse model of AD. Design and method: We studied the effect of 2 months of induced hypertension (AngII-infusion using osmotic micropumps, vs saline (sal) as control) and, subsequently (after 1 month of induced hypertension) the effect of treatment (vs placebo) with antihypertensive (eprosartan mesylate (EM), 0.35 mg/Kg vs water) on SBP and metabolite levels, functional and neuronal connectivity and CBF in 10 months-old wildtype C57bl6/j (WT) and APP/PS1 mice. SBP was monitored twice a month via tail cuff plethysmography. RsfMRI, DTI, MRS, FAIR-ASL were measured on the 11.7T magnet (Bruker BioSpec). Results: In this study, chronic AngII-infusion increased BP in both transgenic and WT mice, while at 12-Month under AngII-infusion APP/PS1 mice had a higher SBP than WT mice. Furthermore, only in hypertensive AD mice cortical CBF was lowered compared to hypertensive WT mice. Additional data will be presented on the impact of AngII-induced hypertension and subsequent treatment with EM on Aβ-pathology, cognition, metabolite levels, structural and functional connectivity. Conclusions: Together, these data suggest an interaction between APP/PS1 induced pathologies, SBP, and antihypertensive treatment. Our results also reveal an association between hypertension (AngII), APP/PS1 and CBF.

Beyond birth-weight: early growth and adolescent blood pressure in a Peruvian population.

Background. Longitudinal investigations into the origins of adult essential hypertension have found elevated blood pressure in children to accurately track into adulthood, however the direct causes of essential hypertension in adolescence and adulthood remains unclear.Methods. We revisited 152 Peruvian adolescents from a birth cohort tracked from 0 to 30 months of age, and evaluated growth via monthly anthropometric measurements between 1995 and 1998, and obtained anthropometric and blood pressure measurements 11–14 years later. We used multivariable regression models to study the effects of infantile and childhood growth trends on blood pressure and central obesity in early adolescence.Results. In regression models adjusted for interim changes in weight and height, each 0.1 SD increase in weight for length from 0 to 5 months of age, and 1 SD increase from 6 to 30 months of age, was associated with decreased adolescent systolic blood pressure by 1.3 mm Hg (95% CI −2.4 to −0.1) and 2.5 mm Hg (95% CI −4.9 to 0.0), and decreased waist circumference by 0.6 (95% CI −1.1 to 0.0) and 1.2 cm (95% CI −2.3 to −0.1), respectively. Growth in infancy and early childhood was not significantly associated with adolescent waist-to-hip ratio.Conclusions. Rapid compensatory growth in early life has been posited to increase the risk of long-term cardiovascular morbidities such that nutritional interventions may do more harm than good. However, we found increased weight growth during infancy and early childhood to be associated with decreased systolic blood pressure and central adiposity in adolescence.

Circulating Aminopeptidase Activities in Men and Women with Essential Hypertension

Essential hypertension is one of the major contributors to premature morbidity and mortality due to the incresased risk for coronary heart disease, stroke, renal disease, peripheral vascular disease and vascular dementia for both men and women. However, its basic causes remain unknown. In the present work we studied the activity of several proteolytic regulatory enzymes related to renin-angiotensin-system (RAS) (aminopeptidase A, APA; aminopeptidase N, APN; aminopeptidase B, APB; and insulin-regulated aminopeptidase, IRAP); with oxytocin regulation (oxytocinase); with the metabolism of GnRH and TRH (pyrrolidone carboxypeptidase, Pcp); and with enkephalins metabolism (enkephalindegrading activity, EDA), to elucidate their role in the mechanisms responsible of essential hypertension and to discuss the possible gender differences. Serum samples of 53 individuals with essential hypertension and 60 healthy volunteers were collected and used to assay enzyme activities, gonad hormones testosterone and estradiol, TSH and free thyroxin (fT4). Differences were observed in APA, APN, Pcp and EDA specific activities, and in serum gonad hormone levels between hypertensive and control groups. Only Pcp activity showed gender differences. Regarding the RAS, APA is reduced while APN is increased, suggesting increased levels of angiotensin II and a facilitation of the conversion of angiotensin III in angiotensin IV. Thus, the changes in several RAS-regulating specific activities and other enzyme activities involved in the neuroendocrine modulation of gonad and stress-related functions are related to essential hypertension with minor gender differences. Therefore, aminopeptidases constitute new elements for the knowledge of the causes of essential hypertension and an alternative as therapeutic targets against the illness.

Clinical Implications

HomeHypertensionVol. 62, No. 1Clinical Implications Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBClinical Implications Originally published1 Jul 2013https://doi.org/10.1161/HYP.0b013e31829d4408Hypertension. 2013;62:2Angiotensinogen Expression in Human Adipose Tissue (page 41)Blood pressure is a heritable trait; the genetic causes of essential hypertension remain unclear. Despite being the first gene linked to hypertension, the importance of polymorphisms in angiotensinogen, the precursor to angiotensin-II, remains controversial. The renin–angiotensin system has both endocrine and intracrine functions controlling arterial pressure. The mechanisms regulating angiotensinogen expression is complicated. Because sequence variants in the promoter may differentially affect transcription factor binding, the mechanisms regulating angiotensinogen may differ depending on the polymorphism(s) carried. The current issue of Hypertension reports an effective strategy to examine whether variation in the angiotensinogen promoter effects its expression through differential binding of transcription factors in adipose tissue. The investigators report increased expression of angiotensinogen mRNA and binding of the transcription factor USF2 in chromatin specifically from the −20C allele in subcutaneous adipose tissue from subjects heterozygous for the −20A/C alleles of angiotensinogen. Thus, subjects carrying high-expressing alleles may have increased levels of angiotensinogen and angiotensin-II in some fat depots. This may be clinically important because circulating angiotensinogen derived from adipose tissue is increased in obesity and evidence implicates a role for angiotensin-II derived from adipose angiotensinogen in the regulation of metabolism and blood pressure. Consequently, further studies will need to assess whether this and other polymorphisms control the level of angiotensin-II in hypertensive and obese subjects.Download figureDownload PowerPointCD8+ T Cells and Chemokines in Human Hypertension (page 126)The pathogenic role of T cells in the development of hypertension has been well documented in animal studies. However, the existence of T-cell–driven inflammation in human hypertension has not been demonstrated. In this issue of Hypertension, Youn et al reported an increased fraction of immunosenescent, proinflammatory, cytotoxic CD8+ T cell, and increased circulating levels of T cell chemokines (MIG, IP-10, and I-TAC) in patients with hypertension. In patients with hypertensive nephrosclerosis, I-TAC was expressed more abundantly in the proximal and distal tubules. This evidence, along with an increased level of serum granzyme B, supports the increased activity of cytotoxic T cells in human hypertension. The authors provide evidence for the first time in favor of the existence of T-cell–driven inflammation in human hypertension.Download figureDownload PowerPointCardiac Effects of Hyperaldosteronism (page 62)Affecting >11% of the patients referred to specialized hypertension centers, primary aldosteronism (PA) is the most common endocrine cause of high blood pressure. Furthermore, it induces cardiovascular damage in excess of that expected based on the degree of blood pressure elevation. PA is potentially curable with a targeted treatment, but whether normalization of the blood pressure and regression of associated cardiovascular damage could be achieved in the long term remained uncertain. Rossi et al prospectively assigned 180 PA patients to either adrenalectomy (n=110) or medical therapy (n=70), based on whether there was lateralization of aldosterone excess at adrenal vein sampling. Long-term follow-up study with serial echocardiography evaluations showed for the first time in a prospective study that atrial fibrillation was ≈6-fold higher in PA than in essential hypertensive patients. After treatment blood pressure fell comparably in adrenalectomized and medically treated PA, as it did in optimally treated essential hypertensives. Left ventricular (LV) mass index and the rate of LV hypertrophy also fell mainly through LV inward remodeling in PA patients. Notwithstanding this, the rate of LV mass that was disproportionally elevated for cardiac workload and sex in PA subjects unexpectedly increased. While highlighting the cardiovascular consequences of PA patients, these findings underscore the importance of a timely identification of PA to enable reversal of the LV abnormalities and lowering cardiovascular risk.Download figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetails July 2013Vol 62, Issue 1 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/HYP.0b013e31829d4408 Originally publishedJuly 1, 2013 PDF download Advertisement

Epigenetic-induced dysregulation of arteriolar vasomotion as a possible cause of essential hypertension and therapeutic importance of Mg ions

Epigenetic-induced dysregulation of arteriolar vasomotion as a possible cause of essential hypertension and therapeutic importance of Mg ions

The role of the endogenous antioxidant enzymes and malondialdehyde in essential hypertension.

Oxidative Stress is caused by an imbalance between the production of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates. 1. To compare the levels of Malondialdehyde (MDA), in hypertensive and normotensive subjects. 2. To compare the levels of the antioxidant enzymes, namely, Catalase, Glutathione peroxidase (GPX) and Superoxide Dismutase (SOD) in hypertensive and normotensive subjects. 3. To determine the correlation between the MDA levels and the mean arterial pressure (MAP) among hypertensive subjects. 4. To determine the correlation between the antioxidant enzyme levels and MAP among the hypertensive subjects and to evaluate the effect of 6 months of antihypertensive therapy with a tight blood pressure control on the MDA levels. Materials and Methods : In this cross sectional study, 25 normotensive and 40 hypertensive subjects were recruited. The hypertensive subjects were further subdivided into three subgroups: Prehypertensives, Stage I hypertensives and Stage II hypertensives. All the subjects underwent a blood pressure measurement and the markers of oxidative stress in their sera were estimated. The subjects of Stage I hypertension and Stage II hypertension were given antihypertensive treatment for 6 months and their blood pressures were tightly regulated and brought to the normotensive state. After 6 months, the estimations of the markers of oxidative stress were done again. The MDA levels were significantly increased in the stage I and stage II hypertension groups as compared to those of the control group (p<0.05). The antioxidant enzymes (SOD, Catalase and GPX) were significantly decreased (p<0.05) in the prehypertension and in the stage I and stage II hypertension groups as compared to those in the control group. There was a significant increase in the levels of the antioxidant enzymes after 6 months of a tight regulation and bringing of the blood pressure to the normotensive state by giving antihypertensive therapy. On comparison of the present study with other studies in which the use of antioxidants were found to be ineffective in the blood pressure reduction, it can be concluded that oxidative stress is an effect rather than a cause of essential hypertension.