Related Target Organ Damage Research Articles

Association between gut microbiota and obesity combined with high carotid intima-media thickness among Chinese children.

Obesity and related target organ damage such as high carotid intima-media thickness (cIMT) in children is associated with cardiovascular disease (CVD) later in life. However, the asso-ciation between gut microbiota and obesity combined with high cIMT among children remains unclear. Therefore, we compared differences in composition, community diversity, and richness of gut microbiota among normal children and obesity combined with or without high cIMT to identify differential microbiota biomarkers. A total of 24 children with obesity combined with high cIMT (OB+high-cIMT), 24 with obesity but normal cIMT (OB+non-high cIMT), and 24 with normal weight and normal cIMT aged 10-11 years matched by age and sex from the "Huantai Childhood Cardiovascular Health Cohort Study" were included. All included fecal samples were tested using 16S rRNA gene sequencing. The community richness and diversity of gut microbiota in OB+high-cIMT children were decreased compared with OB+non-high cIMT children and normal children. At the genus level, the relative abundances of Christensenellaceae_R-7_group, UBA1819, Family_XIII_AD3011_group, and unclassi-fied_o_Bacteroidales were associated with reduced odds of OB+high-cIMT among children. Receiver operating characteristic (ROC) analysis showed that combined Christensenellaceae_R-7_group, UBA1819, Fami-ly_XIII_AD3011_group, and unclassified_o_Bacteroidales performed a high ability in identifying OB+high-cIMT. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) showed that several pathways such as biosynthesis of amino acids and aminoacyl-tRNA pathways were lower in the OB+high-cIMT group compared with the normal group. We found that the alteration of gut microbiota was associated with OB+high-cIMT among children, which indicates that the gut microbiota may be a marker for obesity and related cardiovascular damage among children.

Esansiyel Hipertansiyonlu Çocuklarda Renalaz Seviyeleri

Objective: Left ventricular hypertrophy is the most commonly studied index for hypertension related target organ damage due to the wide usage of echocardiography. Renalase is a monoamine oxidase, mainly produced by the kidneys, regulating blood pressure by reducing catecholamines and acting on cardiovascular functions. In this study, the relationship between serum renalase level and hypertensive cardiac changes in children with essential hypertension was compared with the healthy control group. Materials and Methods: A total of 60 hypertensive children (female/male 20/40) aged between 4-18 years (mean 15.1 ± 1.9 years) were included in the study. Twenty healthy children with normal body mass index (4-18, mean14.2 ± 1.3 years) and similar gender (female/male 10/10) formed the control group. In 30 of hypertensive children (female/male: 9/21), echocardiography showed left ventricular hypertrophy. Echocardiographic findings of 30 remaining hypertensive patients (female/male: 11/19) were normal. A venous blood sample was collected from the hypertensive groups for biochemical examinations and renalase level. Urine samples and 24-hour urine samples were collected. 24-hour ambulatory blood pressure monitoring (ABPM) was used to measure blood pressure of hypertensive groups. The cardiac evaluation of hypertensive groups was performed using M-mode echocardiography. Results: The body mass index was significantly higher in hypertensive groups than the group with normal blood pressure (p <0.05). In comparison of hypertensive groups, no significant difference was found in terms of body mass index. All day systolic, diastolic; night systolic, diastolic, and daytime systolic blood pressure loads were significantly higher in hypertensive left-ventricular hypertrophic group than hypertensive non-hypertrophic group (p <0.05). Left ventricular mass index in M-mode echocardiography, revealed 39.7 g/m2 in the left ventricular hypertrophic group and 27.9 g/m2 in the hypertensive non-hypertrophic group (p <0.05). When the relationship between blood pressure loads and left ventricular mass index was compared between the groups, a significant correlation was found between daytime systolic blood pressure load and increased left ventricular mass index (p <0.05). Renalase level was significantly lower in hypertensive groups compared to normotensive group (p <0.05). There is a relationship between renalase deficiency and increased left ventricular mass index. Conclusion: There is a correlation between renalase deficiency and increased left ventricular mass index. We believe that utilization of low renalase levels as an early marker may be a useful and valuable parameter for determining the patients at risk for left ventricular hypertrophy and long-term complications of hypertension

The role of complement pathway-mediated inflammation and immune regulation in the development of hypertension and related target organ damage

<p indent="0mm">Hypertension is one of the major risk factors for cardiovascular and cerebrovascular diseases. However, the molecular and pathological mechanism of hypertension remains unclear. Recent studies suggest that immune cell activation is involved in the development of hypertension, and chronic low-grade inflammation induces vascular dysfunction and related diseases. The complement pathway, as an important regulator of the immune system, plays a critical role in recruiting immune cells, regulating inflammation and inflammatory factors release. Abnormal activation of complement pathway and up-regulation of complement molecules are involved in the process of hypertension-related cardiovascular diseases. We herein mainly review the role of complement pathway in hypertension and related target organ damage, and propose a potential target for translational research in cardiovascular immunology.

Effects of inhibition of the renin-angiotensin system on hypertension-induced target organ damage: clinical and experimental evidence.

The dysregulation of renin-angiotensin-system (RAS) plays a pivotal role in hypertension and in the development of the related target organ damage (TOD). The main goal of treating hypertension is represented by the long-term reduction of cardiovascular (CV) risk. RAS inhibition either by angiotensin converting enzyme (ACE)-inhibitors or by type 1 Angiotensin II receptors blockers (ARBs), reduce the incidence of CV events in hypertensive patients. Actually, ACE-inhibitors and ARBs have been demonstrated to be effective to prevent, or delay TOD like left ventricular hypertrophy, chronic kidney disease, and atherosclerosis. The beneficial effects of RAS blockers on clinical outcome of hypertensive patients are due to the key role of angiotensin II in the pathogenesis of TOD. In particular, Angiotensin II through an inflammatory-mediated mechanism plays a role in the initiation, progression and vulnerability of atherosclerotic plaque. In addition, Angiotensin II can be considered the hormonal transductor of the pressure overload in cardiac myocytes, and through an autocrine-paracrine mechanism plays a role in the development of left ventricular hypertrophy. Angiotensin II by modulating the redox status and the immune system participates to the development of chronic kidney disease. The RAS blocker should be considered the first therapeutic option in patients with hypertension, even if ACE-inhibitors and ARBs have different impact on CV prevention. ARBs seem to have greater neuro-protective effects, while ACE-inhibitors have greater cardio-protective action.

BCL11B Regulates Arterial Stiffness and Related Target Organ Damage.

[Figure: see text].

AZELNIDIPINE: A REVIEW ON THERAPEUTIC ROLE IN HYPERTINSION

Hypertension is the most common regulating risk factor for cardiovascular disease (CVD) and death; the increased risk associated with blood pressure (BP) elevation can be greatly reduced by treatment with antihypertensive drugs that lower both BP and related target organ damage. New Ca2+ channel antagonists have been recently developed, especially in the DHP compounds that have considerable higher vascular selectivity, slower onset and longer duration of hypotensive action. The antihypertensive effect of azelnidipine is primarily based on the inhibition of trans-membrane Ca2+ influx through the voltage-dependent channels of vascular smooth muscles. Ca2+ channels are categorized into several subtypes, including L-type, T-type, N-type, P/Q-type, and R-type Ca2+ channels depend on their electrophysiological properties. Clinical studies have demonstrated that azelnidipine markedly reduced heart rate and proteinuria in hypertensive patients by inhibiting sympathetic nerve activity. Azelnidipine has also been confirmed to have cardio-protective, neuroprotective, and anti-atherosclerotic properties, and has also been found to prevent insulin resistance.

Association of Urinary Albumin with Selected Cardiovascular Disease Risk Factors in Obese Adolescents

Background: Childhood obesity has become a growing health problem in Egyptand other countries in the world. The prevalence of albuminuria is higher in obesity,and could represent an early indicator for cardiovascular diseases (CVD) in obeseadolescents. Whether there is a real association between albuminuria and other CVDrisk factors remains a matter of debate.Purpose: In an attempt to answer this debate question, this study aims to assessthe association of urinary albumin with central obesity, blood pressure, fasting lipidprofile, and insulin resistance in obese adolescents.Methods: Forty obese adolescents aged 10-18 years, diagnosed with simple obesitywere recruited from the National Nutrition Institute in Egypt. Exclusion criteria wereadolescents with diabetes, kidney or liver prob-lems, and/or hormonal abnormalities.Measurements included anthropometric assess-ment, blood pressure measurement;and lab analysis for urinary albumin, fasting blood glucose, fasting insulin, and fastinglipid profile. The Spearman correlation coefficient was used for statistical analysis.Results: Statistically significant p ositive c orrelations h ave b een f ound o nly betweenalbuminuria and each of: duration of obesity (r=0.93, p= 0.00), waist/height ratio(r=0.65, p=0.00), and/or systolic blood pressure (r=0.33, p= 0.041).Conclusions: Urinary albumin has been significantly a ssociated w ith t he long-termexposure to excess body weight, central fatness, and systolic blood pressure, but notwith diastolic blood pressure, dyslipidemia or insulin resistance in obeseadolescents. Early detection of al-buminuria can have a protective role againstfuture hypertension and related target organ damage in this young population. Theobservations of our study may aid efforts directed to planning better health caresystem for obese children and/or adolescents in Egypt.

A6321 Complement in Hypertension and Target Organ Damage

Objectives: Immunity and inflammation play pivotal roles in the development of hypertension, including innate and adaptive immunity. Complement system provides a bridge between innate and adaptive immune cells. We aim to elucidate the mechanism of complement activation in hypertension and related target organ damage. Methods: Complement C3, C3aR, C5aR knock out (KO) mice were utilized for performing hypertension model, including deoxycorticosterone acetate (DOCA)/salt and angiotensin II (Ang II)-induced hypertension. Macrophage and T cells were separated for stimulating with complement factors. Results: We firstly found that perivascular adipose tissue (PVAT) expressed abundant C3, which stimulated adventitial fibroblast migration and phenotype transdifferentiation. Subsequently, we showed that C5a regulated M1/M2 macrophage polarization and inhibited adiponectin production in the PVAT, which contributed to vascular inflammation in hypertension. More important, we demonstrated that double C3aR and C5aR KO (DKO) prevented Ang II-induced blood pressure elevation. Mechanically, DKO activated the immunosuppressive functio of regulatory T cells (Tregs). Adoptive transfer of DKO Tregs attenuated Ang II-induced hypertension and target organ damage. Conclusion: Our results demonstrate that complement activation-mediated immune cell infiltration is involved in the development of hypertension and target organ damage. Blockade of complement activation may be an alternative novel approach for hypertension treatment.

Abstract P231: Circulatory Gene Regulation in Youth With Primary Hypertension and Target Organ Damage

Introduction: Primary hypertension (PH) is a multifactorial disease mainly influenced by genetic, epigenetic and environmental dynamics. Despite the occurrence of PH-associated cardiovascular (CV) events in youth, we have acquired only a limited understanding of epigenetic and gene regulation of blood pressure (BP)-related target organ damage (TOD) in adolescents. Aims and Objectives: To define circulatory gene and miRNA expression levels and allied signaling pathways in hypertensive adolescents (Hyp) with TOD. Methods and Results: Three hundred adolescents of both genders aged 11 to 18 years participated in the AHA-funded Study of Hypertension in Pediatrics - Adult Hypertension Onset in Youth (SHIP AHOY) Project. Mean clinic SBP was 104.3 ±8.1 and 133.0 ± 8.2 mmHg in normal vs Hyp ( p&lt;0.005 ) and mean daytime ambulatory SBP was 115.7 ±11.4 and 128.9 ±6.4 mmHg in normal vs Hyp ( p&lt;0.005 ), respectively. Youth with PH also had higher BMI (22.33 ±3.67 vs 31.56 ±9.42; p&lt; 0.05 ), elevated serum creatinine (0.73 ± 0.18 vs 0.92 ±0.12; p&lt; 0.05 ), and left ventricular hypertrophy (LVM/ht 2.7 ; 25.4 ±1.8 vs 41.7 ±1.8; p&lt; 0.05 ), and trend for increased arterial stiffness (PWV; 4.8 ±0.6 vs 5.8 ±2.0; p =0.18). mRNA and microRNA seq were performed using peripheral blood cells of 10 normal (mean 15.2 ±1.4 years; 50% male), and 10 Hyp patients (mean 15.5 ±1.5 years; 70% male). Seq data analysis revealed master genes (Fig. 1) and pathways that were differentially regulated in Hyp patients with TOD. Conclusions: PH in youth is associated with TOD that relates to a distinct gene expression profile. Knowledge of allied pathways may lead to new treatments in hypertensive youth to prevent future CV diseases.

Brain MRI fiber-tracking reveals white matter alterations in hypertensive patients without damage at conventional neuroimaging

Hypertension is one of the main risk factor for dementia. The subtle damage provoked by chronic high blood pressure in the brain is usually evidenced by conventional magnetic resonance imaging (MRI), in terms of white matter (WM) hyperintensities or cerebral atrophy. However, it is clear that by the time brain damage is visible, it may be too late hampering neurodegeneration. Aim of this study was to characterize a signature of early brain damage induced by hypertension, before the neurodegenerative injury manifests. This work was conducted on hypertensive and normotensive subjects with no sign of structural damage at conventional neuroimaging and no diagnosis of dementia revealed by neuropsychological assessment. All individuals underwent cardiological clinical examination in order to define the hypertensive status and the related target organ damage. Additionally, patients were subjected to DTI-MRI scan to identify microstructural damage of WM by probabilistic fiber-tracking. To gain insights in the neurocognitive profile of patients a specific battery of tests was administered. As primary outcome of the study we aimed at finding any specific signature of fiber-tracts alterations in hypertensive patients, associated with an impairment of the related cognitive functions. Hypertensive patients showed significant alterations in three specific WM fiber-tracts: the anterior thalamic radiation, the superior longitudinal fasciculus and the forceps minor. Hypertensive patients also scored significantly worse in the cognitive domains ascribable to brain regions connected through those WM fiber-tracts, showing decreased performances in executive functions, processing speed, memory, and paired associative learning tasks. Overall, WM fiber-tracking on MRI evidenced an early signature of damage in hypertensive patients when otherwise undetectable by conventional neuroimaging. In perspective, this approach could allow identifying those patients that are in initial stages of brain damage and could benefit of therapies aimed at limiting the transition to dementia and neurodegeneration.

The Use of Ambulatory Blood Pressure Monitoring As Standard of Care in Pediatrics.

Hypertension (HTN) is a significant global health problem, responsible for 7.5 million deaths each year worldwide. The prevalence of HTN is increasing in the pediatric population likely attributed to the increase in childhood obesity. Recent work has also shown that blood pressure (BP) tends to track from childhood to adulthood including BP-related target organ damage. In the last 25–30 years, pediatric use of ambulatory blood pressure monitoring (ABPM) has been expanding mainly in the setting of initial elevated BP measurement evaluation, HTN therapy efficacy follow-up, and renal disease. However, there are many clinical areas where ABPM could potentially be used but is currently underutilized. This review summarizes the current knowledge and the uses of pediatric ABPM and explores clinical areas where it can be very useful both to detect HTN and its longitudinal follow-up. And thus, ABPM could serve as a critical tool to potentially prevent early cardiovascular mortality and morbidity in wide variety of populations. With solid data to support ABPM’s superiority over clinic BP measurements and these clinical areas for its expansion, ABPM should now be part of standard of care in BP evaluation and management in pediatrics.

Role of biological sex in cardiovascular disease: the case of hypertension and related target organ damage

Individual characteristics, such as age, biological sex, race, fat mass and genetic factors, have a major impact on physiological and pathological processes. Consequently, individuals can respond differently to the development and manifestation of disease, treatment, outcome and the recovery process. In fact, there are major differences in the function of the biological system of men and women, who do not differ only on the basis of their reproductive system. Sex chromosomes and sex hormones, together with other factors, interact in a complex manner, thereby leading to sex-specific protective or maladaptive mechanisms. In this context, studying the role and effects of biological sex is crucial for the identification of novel therapeutic targets, whose therapeutic exploitation will promote a personalized and improved treatment and care according to individual needs. The vast influence of biological sex is recognized in many diseases1. Here, we focus on hypertension, due to its high prevalence and importance, since it is the primary risk factor for premature death and disability worldwide.

Eating frequency predicts new onset hypertension and the rate of progression of blood pressure, arterial stiffness, and wave reflections.

Cross-sectional evidence indicates that eating frequency correlates with blood pressure, hypertension, and related target organ damage. The aim of the present study was to prospectively assess eating frequency as a predictor of arteriosclerosis progression and new onset hypertension over a follow-up period of 5 years in adults without cardiovascular disease. Eating frequency among other dietary parameters was evaluated in 115 nondiabetic study participants from a general population sample (54 ± 9.1 years, 45 women) at a baseline visit. Metabolic parameters known to be associated with eating frequency, markers of arteriosclerosis, including augmentation index, pulse wave velocity, SBP, and DBP were evaluated in all volunteers at baseline and after a 5-year follow-up. By applying linear mixed models analysis, it was found that a high eating frequency at baseline significantly correlated with the rate of progression of pulse wave velocity (β = 0.521, P = 0.004), augmentation index (β = 0.503, P = 0.01), SBP (β = 0.694, P < 0.001), and DBP (β = 0.477, P = 0.009) and the incidence of new onset hypertension (odds ratio = 8.89, P < 0.001). After adjustment traditional cardiovascular risk factors, heart rate, homeostasis model assessment index of insulin resistance and total energy intake, the associations with augmentation index, SBP, DBP, and new onset hypertension remained significant. In a population of nondiabetic adults without cardiovascular disease, eating frequency is associated with the rate of progression of wave reflections, blood pressure and of new onset hypertension. Interventional studies should confirm these data and possibly further assess the utility of eating behavior in the prevention of new onset hypertension and related target organ damage.

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Hypertension is one of the most common disease afflicting humans throughout the world. Target organ damage resulting from hypertension includes those affecting the brain, heart, kidneys and the eyes. Focal neurological deficits, dyspnoea, chest pain, headache, loss of vision are considered as the commonest symptoms with which patients having hypertension related acute target organ damage present. OBJECTIVES To assess the prevalence of micro-albuminuria among the non-diabetic hypertensive patients and to assess the relationship between micro-albuminuria and target organ damage. MATERIALS AND METHODS A cross-sectional study was conducted in 100 hypertensive patients microalbuminuria was measured in these patients by micral dipstick method. Chi-square test was used to study the relationship between microalbuminuria and other variables. P value was calculated for all the variables. RESULTS The prevalence of microalbuminuria was 23% among the non-diabetic hypertensive patients. A positive correlation between microalbuminuria and target organ damage was found in these patients. The odds ratio for microalbuminuric patients having retinopathy was 8.3% (95% confidence interval 2.4-37.5). Prevalence of microalbuminuria was higher among patients with Cerebrovascular Accidents (P < 0.001) with the odds ratio of 15.3 (95% confidence interval 4.9-47.5) and it was observed that there was significant correlation between the prevalence of microalbuminuria and the presence of LVH (P <0.001) with the odds ratio of 10.4 (95% confidence interval 3.52-30.8) in hypertensive patients. CONCLUSION

Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology.

Exaggerated activation of the renin-angiotensin system via tissue angiotensin II (Ang II) type 1 receptor (AT1R) signaling exerts detrimental effects on cardiovascular, renal and endocrine systems to provoke hypertension and related target organ damage. On the other hand, accumulated research evidence of both basic and clinical studies shows that physiological AT1R signaling also plays an indispensable role for the normal organ development such as the kidney and the maintenance of cardiovascular and renal homeostasis. Such functional diversity of AT1R signaling prompts us to seek a new strategy of selective modulation of AT1R signaling in pathophysiology. In the course of an investigational search for a means to functionally and selectively modulate AT1R signaling for that purpose, a molecule directly interacting with the carboxyl-terminal cytoplasmic domain of AT1R was identified by employing yeast two-hybrid screening of a mouse kidney cDNA library and named AT1R-associated protein (ATRAP). The results of functional analysis showed that ATRAP promotes constitutive AT1R internalization in cultured cells and inhibits Ang II-mediated pathological response in mouse distal convoluted cells. The ATRAP is expressed in a variety of tissues including the kidney where ATRAP is abundantly distributed in epithelial cells along the renal tubules. The results employing genetic engineered mice with modified ATRAP expression showed that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli such as chronic Ang II infusion, and suggest ATRAP to be a target of interest.

Differential modulation of AMPK/PPARα/UCP2 axis in relation to hypertension and aging in the brain, kidneys and heart of two closely related spontaneously hypertensive rat strains.

We examined expression protein of AMPK/SIRT1/PGC1α/PhoxO3a/PPARα/UCP2 pathway in brain, kidneys and heart of stroke-prone spontaneously hypertensive rat (SHRSP) vs stroke-resistant SHR (SHRSR) at different weeks of age, up to one year, in order to test the hypothesis that abnormalities within this pathway could associate with higher susceptibility of SHRSP to develop hypertension-related vascular damage. SHRSP develops severe hypertension and related target organ damage. Marked reduction of uncoupling protein 2 (UCP2) expression upon high salt-low potassium diet associates with increased renal injury in SHRSP. UCP2 may represent a key mitochondrial protein involved in cardiovascular damage. At 2 months of age a significant down-regulation of UCP2 expression at both mRNA and protein levels was found, along with reduced protein expression of all components of UCP2 regulatory pathway, in tissues of SHRSP but not of SHRSR, that progressed with hypertension development and aging. A significant increase of both oxidative stress and inflammation was detected in tissues of SHRSP as a function of age. SBP levels were significantly higher in SHRSP than SHRSR at 3 months of age and thereafter. At one year of age, higher degree of renal damage, with proteinuria and severe glomerular and tubulo-interstitial fibrosis, of cerebral damage, with significant vessel extravasation and stroke occurrence, and of myocardial damage was detected in SHRSP than SHRSR. The early significant reduced expression of the antioxidant AMPK/PPARα/UCP2 pathway that progressed throughout lifetime may contribute to explain higher predisposition of SHRSP to oxidative stress dependent target organ damage in the context of severe hypertension.

Specific genetic influences on nighttime blood pressure.

Nighttime blood pressure (BP) has been shown to be superior to daytime BP in predicting hypertension related target organ damage and cardiac mortality. In our Georgia Cardiovascular Twin Study, we showed that apart from the genes that also influence daytime BP, specific genetic determinants explained 44% and 67% of the nighttime systolic BP (SBP) and diastolic BP (DBP) heritabilities, respectively. Here, we determined whether these results could be confirmed in a much larger twin cohort of young adults with 24-hour ambulatory BP measurements. Ambulatory BP was available in 703 white twins (308 pairs and 87 singletons, aged 18-34 years, 50% males) from the Prenatal Programming Twin Study. A bivariate quantitative genetic twin model was used to analyze daytime and nighttime BP. We conducted a meta-analysis to compare and integrate results from the 2 twin cohorts. Model fitting showed no sex differences for any of the measures. Heritabilities were 0.60 and 0.51 for SBP and 0.54 and 0.46 for DBP at daytime and nighttime. The specific heritability due to novel genetic effects emerging during the nighttime was 0.21 for SBP and 0.26 for DBP, which comprised 41% and 57% of the total nighttime heritability for SBP and DBP, respectively. Meta-analysis confirmed absence of cohort differences with very similar combined results. In addition to genes that influence both daytime and nighttime BP, a large part of the heritability is explained by genes that specifically influence BP at night.

English

BACKGROUND AND OBJECTIVES: The clinical profile of patients with hypertensive emergencies presenting to rural hospitals in a developing country like ours is unknown. The objective of the present study was to evaluate the modes of presentations, clinical profile and spectrum of target organ damage in patients with hypertensive emergencies. METHOD: This observational study was done at SRI ADICHUNCHANGIRI INSTITUTE OF MEDICAL SCIENCES AND REASEARCH CENTER over a period of one and a half years. The study population included patients admitted to this hospital with severely elevated blood pressure with clinical or laboratory evidence of acute target organ damage. The clinical and laboratory profile of 50 patients were evaluated. RESULTS: Males had higher chances of developing a hypertensive emergency compared to females, male: female ratio 2.57:1. The commonest presenting symptoms were neurological deficit (50%), dyspnea (30%), followed by chest pain (24%). Majority of the patients were known hypertensive (70%). Higher levels of blood pressure at presentation were associated with an adverse outcome. Laboratory abnormalities noticed in these patients included hyponatremia and hyperkalemia. Acute intracerebral hemorrhage was the commonest mode of target organ damage. An in hospital mortality of 24% was observed in the present study. INTRODUCTION: Hypertension affects individuals of all classes and across all age groups. The prevalence of hypertension increases with advancing age to the point where more than half of people of 60–69 years of age and approximately three-fourths of those 70 years of age and older are affected.1 The age related rise in SBP is primarily responsible for an increase in both incidence and prevalence of hypertension with increasing age.1 The relationship between blood pressure and risk of cardiovascular disease events is continuous, consistent and independent of other risk factors.1 Hypertension affects approximately one billion individuals worldwide as per the observations made by the Joint national committee on prevention, detection, evaluation and treatment of high blood pressure (JNC VII) report in 2003.1 Higher than optimal blood pressure is the number one attributable risk for death throughout the world and approximately 7.1 million deaths per year are attributed to uncontrolled hypertension.2 Target organ damage resulting from hypertension includes those affecting the brain, heart, kidneys and the eyes. A number of cardiovascular, pulmonary and neurological symptoms are found to be associated with patients in hypertensive emergency with target organ involvement.3 Focal neurological deficits, dyspnea, chest pain, headache, loss of vision, are considered as the commonest symptoms with which patients in hypertension related acute target organ damage present.3 As population ages the prevalence of hypertension will increase even further unless broad and effective preventive measures are implemented.1 DOI: 10.14260/jemds/2014/2693

English

Metabolic and humoral mechanisms have been known to be involved in the development and progression of cardiovascular-related sympathetic overdrive. Sympathetic overactivity in the genesis of major complications of cardiovascular system and associated organ damages has been reported as one of the major participant. Evidences has been provided that sympathetic neural mechanisms may participate in the development of cardiovascular -related target organ damage, such as left ventricular hypertrophy, diastolic dysfunction, impaired arterial compliance vascular atherosclerosis and renal failure. Renalase, a circulating FAD-dependent amine oxidase, has been reported as a secretion in blood form the kidney as well as from heart, skeletal muscle and small intestine and known to alter systemic blood pressure, cardiac & renal function in health and diseases. It has been identified in two isoforms of the human protein and is produced by alternative splicing. In vitro studies have demonstrated that Renalase triggers the release as well as degrades catecholamines such as dopamine, norepinephrine and epinephrine and thus has been claimed to have casual link between sympathetic overdrive and increase risk of cardiovascular dysfunction & related organ damage. This paper discussed the main features of physiological functions of renalase, including its sources of secretion, expression and circulating level and their relevance with adrenergic function in cardiovascular dysfunctions & related organ damage. The paper also reviewed the potential role of renalase in the diagnostic and /or therapeutic approach to cardiovascular disorders & renal diseases, aimed at regulation of sympathetic deactivation.

Treatment of resistant hypertension

Treatment of resistant hypertension