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Essential Hypertension (essential + hypertension)
Kinds of Essential Hypertension Selected AbstractsModified TEI Index: A Promising Parameter in Essential Hypertension?ECHOCARDIOGRAPHY, Issue 4 2005Nurgül Keser M.D. Purpose: Modified TEI index is pointed to be more effective in the evaluation of global cardiac functions compared to systolic and diastolic measurements alone. We planned to determine its applicability in hypertension and relation with left ventricular mass index (LVMI). Methods: We studied 48 patients with mild/moderate hypertension and normal coronary angiograms. In total 22 patients (12 men, 10 women, mean age: 55 ± 6) with normal LVMI were studied in group I, 26 patients (12 men, 14 women, mean age: 57 ± 7) with increased LVMI in group II, and 20 patients (10 men, 10 women, mean age: 53 ± 7) with normal blood pressure as a control group. Standard 2D, Doppler, and mitral annulus pulse wave tissue Doppler were used for all measurements. Modified TEI index was calculated as diastolic time interval measured from end of Am wave to origin of Em (a,) minus systolic Sm duration (b,) divided by b(a,,b,/b,). Results: Modified TEI index was significantly higher in both groups than normal group and in group II than in group I. (Control group: 0.33 ± 0.05, group I: 0.51 ± 0.17, group II: 0.68 ± 0.16, P< 0.0001). Conclusion: Modified TEI index, a marker of left ventricular systolic and diastolic functions, is impaired in hypertensives before hypertrophy develops and impairment is more prominent in hypertrophy. Therefore, (1) modified TEI index in hypertensives is a safe, feasible, and sensitive index for evaluation of global ventricular functions. (2) Evaluation of hypertensives with this index periodically may guide interventions directed toward saving systolic and diastolic functions. (3) Modified TEI index is gaining importance as a complementary parameter to standard Doppler or in cases where standard Doppler has its limitations. [source] What Is the Best Drug to Prescribe for a Young Woman in Her Childbearing Years With Essential Hypertension?JOURNAL OF CLINICAL HYPERTENSION, Issue 4 2008Debbie L. Cohen MD No abstract is available for this article. [source] Routine Measurement of Plasma Renin Activity in the Management of Patients With Essential Hypertension: Notes From the 19th Annual ASH MeetingJOURNAL OF CLINICAL HYPERTENSION, Issue 12 2004Ari Mosenkis MD No abstract is available for this article. [source] Aortic Calcification Is Associated With Age and Sex but Not Left Ventricular Mass in Essential HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 2 2004Alexandros Tsakiris MD The aim of this study was to investigate the prevalence of aortic calcification in patients with essential hypertension and its relationship with age, sex, and left ventricular hypertrophy. Two hundred ninety consecutive patients with essential hypertension were studied. A chest radiograph and an echocardiograph were performed. Aortic calcification was observed in 74/290 (25.5%) patients. Patients with calcification were mostly female (67.6%) and older (71.8±1.9 years), whereas patients without calcification were younger (59.0±0.79) and of both sexes (51.85% female). Left ventricular mass index in male patients with aortic calcification was 147.3±4.32 g/m2 and without calcification was 132.7±2.28 g/m2 (p=0.023). Female patients' values were 131.9±4.32 g/m2 with calcification and 121.2±2.85 g/m2 without calcification (p=0.025). Left ventricular mass was independently associated with age and sex but not with aortic calcification. The prevalence of aortic calcification in essential hypertension is considerably higher compared to the general population. Essential hypertension and age seem to contribute to the concurrent appearance of aortic calcification and increased left ventricular mass. [source] G Protein ,3 Subunit Gene Variants and Essential Hypertension in the Northern Chinese Han PopulationANNALS OF HUMAN GENETICS, Issue 4 2005Biao Li Summary Recently a novel C825T polymorphism in the G protein ,3 subunit gene was identified that showed an association with hypertension in a German population; the results of studies in other populations have been inconsistent. To examine the contribution of GNB3 polymorphisms to the development of hypertension in the northern Chinese Han population, we conducted a case-control study consisting of 501 hypertensive cases and 503 controls using the G(-350)A, C825T and C1429T polymorphisms. Genotypes of samples were determined by PCR and restriction digestion. Single locus analysis showed a significant association between G(-350)A and hypertension (P = 0.01) but no association for C825T or C1429T. The three polymorphisms were in tight linkage disequilibrium (D,=,1 for G(-350)A-C825T, D,= 0.92 for C825T-C1429T) and a total of 7 haplotypes were observed in the entire population. Haplotype A-C-C was found to be significantly related to hypertension (P = 0.032) and A-C-C carriers had a more than two-fold higher risk of hypertension than non-carriers, after adjustment for BMI and glucose. In conclusion, our study suggests that G(-350)A is a potential functional polymorphism that may be related to hypertension, whereas the C825T and C1429T polymorphisms are not associated with hypertension in the northern Chinese Han population. [source] Human Chromosome 17 in Essential HypertensionANNALS OF HUMAN GENETICS, Issue 2 2003J. Knight Summary Hypertension affects up to 30% of the adult population in Western societies and is a major risk factor for kidney disease, stroke and coronary heart disease. It is a complex trait thought to be influenced by a number of genes and environmental factors, although the precise aetiology remains unknown at this time. A number of methods have been successfully used to identify mutations that cause Mendelian traits and these are now being applied to the investigation of complex diseases. This review summarises the data gathered, using such approaches, that suggest there is a gene or genes on chromosome 17 causing human essential hypertension. Studies in rodent models are discussed first, followed by studies of human hypertension that include the investigation of pseudohypoaldosteronism type II, a monogenic trait that manifests with hypertension alongside other phenotypic variables. In addition, candidate gene studies, genome screens and linkage studies based on comparative mapping are outlined. To date no gene has been identified on human chromosome 17 that influences blood pressure and causes human essential hypertension. However, results of ongoing fine mapping and candidate gene studies in both rodents and man are eagerly awaited. [source] Aortic Calcification Is Associated With Age and Sex but Not Left Ventricular Mass in Essential HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 2 2004Alexandros Tsakiris MD The aim of this study was to investigate the prevalence of aortic calcification in patients with essential hypertension and its relationship with age, sex, and left ventricular hypertrophy. Two hundred ninety consecutive patients with essential hypertension were studied. A chest radiograph and an echocardiograph were performed. Aortic calcification was observed in 74/290 (25.5%) patients. Patients with calcification were mostly female (67.6%) and older (71.8±1.9 years), whereas patients without calcification were younger (59.0±0.79) and of both sexes (51.85% female). Left ventricular mass index in male patients with aortic calcification was 147.3±4.32 g/m2 and without calcification was 132.7±2.28 g/m2 (p=0.023). Female patients' values were 131.9±4.32 g/m2 with calcification and 121.2±2.85 g/m2 without calcification (p=0.025). Left ventricular mass was independently associated with age and sex but not with aortic calcification. The prevalence of aortic calcification in essential hypertension is considerably higher compared to the general population. Essential hypertension and age seem to contribute to the concurrent appearance of aortic calcification and increased left ventricular mass. [source] Synthesis and biological evaluation of [carboxyl - 11C]eprosartanJOURNAL OF LABELLED COMPOUNDS AND RADIOPHARMACEUTICALS, Issue 8 2009Ola Åberg Abstract Essential hypertension occurs in approximately 25% of the adult population and one cause of hypertension is primary aldosteronism. Targeting the angiotensin II AT1 receptor using PET and an appropriate tracer may offer a diagnostic method for adrenocortical tissue. This report describes the synthesis of the selective AT1 receptor antagonist [carboxyl - 11C]eprosartan 10, 4-[2-butyl-5-((E)-2-carboxy-3-thiophen-2-yl-propenyl)-imidazol-1-ylmethyl]-[carboxyl - 11C]benzoic acid, and its precursor (E)-3-[2-butyl-3-(4-iodo-benzyl)-3H -imidazol-4-yl]-2-thiophen-2-ylmethyl-acrylic acid 9. 11C-carboxylation of the iodobenzyl moiety was performed using a palladium-mediated reaction with [11C]carbon monoxide in the presence of tetra- n -butyl-ammonium hydroxide in a micro-autoclave using a temperature gradient from 25 to 140°C over 5,min. After purification by semipreparative HPLC, [carboxyl - 11C]eprosartan 10 was obtained in 37,54% decay-corrected radiochemical yield (from [11C]carbon monoxide) with a radiochemical purity >95% within 35,min of the end of bombardment (EOB). A 5-µAh bombardment gave 2.04,GBq of 10 (50% rcy from [11C]carbon monoxide) with a specific activity of 160,GBq,µmol,1 at 34,min after EOB. Frozen-section autoradiography shows specific binding in kidney, lung and adrenal cortex. In vivo experiments in rats demonstrate a high accumulation in kidney, liver and intestinal wall. Copyright © 2009 John Wiley & Sons, Ltd. [source] De novo expression of Kv6.3 contributes to changes in vascular smooth muscle cell excitability in a hypertensive mice strainTHE JOURNAL OF PHYSIOLOGY, Issue 3 2009Alejandro Moreno-Domínguez Essential hypertension involves a gradual and sustained increase in total peripheral resistance, reflecting an increased vascular tone. This change associates with a depolarization of vascular myocytes, and relies on a change in the expression profile of voltage-dependent ion channels (mainly Ca2+ and K+ channels) that promotes arterial contraction. However, changes in expression and/or modulation of voltage-dependent K+ channels (Kv channels) are poorly defined, due to their large molecular diversity and their vascular bed-specific expression. Here we endeavor to characterize the molecular and functional expression of Kv channels in vascular smooth muscle cells (VSMCs) and their regulation in essential hypertension, by using VSMCs from resistance (mesenteric) or conduit (aortic) arteries obtained from a hypertensive inbred mice strain, BPH, and the corresponding normotensive strain, BPN. Real-time PCR reveals a differential distribution of Kv channel subunits in the different vascular beds as well as arterial bed-specific changes under hypertension. In mesenteric arteries, the most conspicuous change was the de novo expression of Kv6.3 (Kcng3) mRNA in hypertensive animals. The functional relevance of this change was studied by using patch-clamp techniques. VSMCs from BPH arteries were more depolarized than BPN ones, and showed significantly larger capacitance values. Moreover, Kv current density in BPH VSMCs is decreased mainly due to the diminished contribution of the Kv2 component. The kinetic and pharmacological profile of Kv2 currents suggests that the expression of Kv6.3 could contribute to the natural development of hypertension. [source] Region-specific changes in sympathetic nerve activity in angiotensin II,salt hypertension in the ratEXPERIMENTAL PHYSIOLOGY, Issue 1 2010John W. Osborn It is now well accepted that many forms of experimental hypertension and human essential hypertension are caused by increased activity of the sympathetic nervous system. However, the role of region-specific changes in sympathetic nerve activity (SNA) in the pathogenesis of hypertension has been difficult to determine because methods for chronic measurement of SNA in conscious animals have not been available. We have recently combined indirect, and continuous and chronic direct, assessment of region-specific SNA to characterize hypertension produced by administration of angiotensin II (Ang II) to rats consuming a high-salt diet (Ang II,salt hypertension). Angiotensin II increases whole-body noradrenaline (NA) spillover and depressor responses to ganglionic blockade in rats consuming a high-salt diet, but not in rats on a normal-salt diet. Despite this evidence for increased ,whole-body SNA' in Ang II,salt hypertensive rats, renal SNA is decreased in this model and renal denervation does not attenuate the steady-state level of arterial pressure. In addition, neither lumbar SNA, which largely targets skeletal muscle, nor hindlimb NA spillover is changed from control levels in Ang II,salt hypertensive rats. However, surgical denervation of the splanchnic vascular bed attenuates/abolishes the increase in arterial pressure and total peripheral resistance, as well as the decrease in vascular capacitance, observed in Ang II,salt hypertensive rats. We hypothesize that the ,sympathetic signature' of Ang II,salt hypertension is characterized by increased splanchnic SNA, no change in skeletal muscle SNA and decreased renal SNA, and this sympathetic signature creates unique haemodynamic changes capable of producing sustained hypertension. [source] Comprehensive linkage and linkage heterogeneity analysis of 4344 sibling pairs affected with hypertension from the Family Blood Pressure ProgramGENETIC EPIDEMIOLOGY, Issue 3 2007Tiffany A. Greenwood Abstract Linkage analyses of complex, multifactorial traits and diseases, such as essential hypertension, have been difficult to interpret and reconcile. Many published studies provide evidence suggesting that different genes and genomic regions influence hypertension, but knowing which of these studies reflect true positive results is challenging. The reasons for this include the diversity of analytical methods used across these studies, the different samples and sample sizes in each study, and the complicated biological underpinnings of hypertension. We have undertaken a comprehensive linkage analysis of 371 autosomal microsatellite markers genotyped on 4,334 sibling pairs affected with hypertension from five ethnic groups sampled from 13 different field centers associated with the Family Blood Pressure Program (FBPP). We used a single analytical technique known to be robust to interpretive problems associated with a lack of completely informative markers to assess evidence for linkage to hypertension both within and across the ethnic groups and field centers. We find evidence for linkage to a number of genomic regions, with the most compelling evidence from analyses that combine data across field center and ethnic groups (e.g., chromosomes 2 and 9). We also pursued linkage analyses that accommodate locus heterogeneity, which is known to plague the identification of disease susceptibility loci in linkage studies of complex diseases. We find evidence for linkage heterogeneity on chromosomes 2 and 17. Ultimately our results suggest that evidence for linkage heterogeneity can only be detected with large sample sizes, such as the FBPP, which is consistent with theoretical sample size calculations. Genet. Epidemiol. 2007. © 2007 Wiley-Liss, Inc. [source] A haplotype of the catalase gene confers an increased risk of essential hypertension in Chinese Han,HUMAN MUTATION, Issue 3 2010Zhimin Wang Abstract Our previous study in an isolated population showed an association between a genetic variant in the catalase gene (CAT) and essential hypertension (EH). This study indicates that three variants in the promoter and 5,-UTR region of CAT are predominant in Chinese Han, and they form two major haplotypes. A case,control study showed that the CATH2 haplotype confers susceptibility to EH (Pgenotype=0.0017, and Pallilc=0.00078). Subjects bearing CATH1/CATH2 and CATH2/CATH2 genotypes demonstrated a higher susceptibility to EH than CATH1/CATH1 homozygotes, with odds ratios of 1.474 and 1.625, respectively. Also, CATH1/CATH1 individuals had a later-onset age (P=0.015). Expression analysis using luciferase reporter vectors indicated that the CATH1 haplotype showed a lower transcriptional activity than the haplotype CATH2 (P<0.05 in all four cell lines), and we observed similar results in the endogenous allelic expression ratios of CATH1/CATH2 in cell lines. In contrast, most CATH1 haplotypes showed a higher transcription level than CATH2 haplotypes (10 out of 11 or 90.9%) in blood from normal individuals (P<0.01). We therefore hypothesize that CATH1 and CATH2 may play alternating roles at different level of oxidative stress. Hum Mutat 31:272,278, 2010. © 2009 Wiley-Liss, Inc. [source] Relationship of serum homocysteine and high sensitivity C-reactive protein in elderly people with essential hypertensionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2010L. Yan-Yan No abstract is available for this article. [source] Effectiveness and safety of eprosartan on pulse pressure for the treatment of hypertensive patientsINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 4 2005N. R. Robles Summary A multicentre, prospective, non-comparative open-label study was conducted to assess the effect of eprosartan, 600 mg/day, on pulse pressure (PP) in patients with hypertension (stage I or II, Joint National Committee, sixth report) treated in the primary care setting, as well as safety and compliance. The duration of treatment was 16 weeks. Eprosartan decreased PP (,13 mmHg), systolic blood pressure (SBP) (,26 mmHg), diastolic blood pressure (DBP) (,13 mmHg) and mean arterial pressure (MAP) (,17.4 mmHg) significantly (p < 0.0001). The PP/MAP ratio changed significantly from 62 to 59%, so that the reduction of PP was 3% higher than the overall decrease in MAP. Twenty adverse events, mostly gastrointestinal complaints, were recorded in 12 patients (1.9%). Compliance with treatment at the end of the study was 94%. Eprosartan was a well-tolerated and an effective drug in reducing PP, SBP and DBP below the recommended levels in patients with mild-to-moderate essential hypertension, allowing a high therapeutic compliance. [source] Aortic Calcification Is Associated With Age and Sex but Not Left Ventricular Mass in Essential HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 2 2004Alexandros Tsakiris MD The aim of this study was to investigate the prevalence of aortic calcification in patients with essential hypertension and its relationship with age, sex, and left ventricular hypertrophy. Two hundred ninety consecutive patients with essential hypertension were studied. A chest radiograph and an echocardiograph were performed. Aortic calcification was observed in 74/290 (25.5%) patients. Patients with calcification were mostly female (67.6%) and older (71.8±1.9 years), whereas patients without calcification were younger (59.0±0.79) and of both sexes (51.85% female). Left ventricular mass index in male patients with aortic calcification was 147.3±4.32 g/m2 and without calcification was 132.7±2.28 g/m2 (p=0.023). Female patients' values were 131.9±4.32 g/m2 with calcification and 121.2±2.85 g/m2 without calcification (p=0.025). Left ventricular mass was independently associated with age and sex but not with aortic calcification. The prevalence of aortic calcification in essential hypertension is considerably higher compared to the general population. Essential hypertension and age seem to contribute to the concurrent appearance of aortic calcification and increased left ventricular mass. [source] Correlates of NT-proBNP concentration in patients with essential hypertension in absence of congestive heart failureJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 1 2010Keizo Toda Abstract Background: N-terminal proBNP (NT-proBNP) is widely used as a diagnostic biomarker and for the risk stratification of patients with heart failure (HF). Its role in the evaluation of patients with essential hypertension (EHT) is less clear. We examined the relationship between NT-proBNP concentrations and various clinical characteristics in hypertensive patients without HF. Methods: This study included 186 consecutive patients with EHT and no history of HF, ischemic heart disease, or atrial fibrillation. Single and multiple variable regression analyses were performed in search of clinical correlates of NT-proBNP concentrations. Results: In patients with EHT, median serum concentration of NT-proBNP was 73,pg/ml, and interquartile range (IQR) was 40,128,pg/ml. NT-proBNP was significantly higher (P<0.001) in women (87,pg/ml; IQR 55,137,pg/ml) than in men (52,pg/ml; IQR 24,115,pg/ml). Age (r=0.371, P<0.001), precordial QRS voltage (r=0.223, P<0.001), hemoglobin (Hgb) concentration, (r=,0.208, P=0.023) and estimated glomerular filtration rate (r=,0.139, P=0.044) were correlated with log-transformed NT-proBNP by multiple variable analysis. In men, age (r=0.453, P<0.001) and QRS voltage (r=0.283, P=0.004), and in women age (r=0.299, P=0.006), QRS voltage (r=0.212, P=0.019), Hgb (r=,0.182, P=0.049), and estimated glomerular filtration rate (r=,0.272, P=0.009) were correlated with serum concentrations of NT-proBNP. Conclusions: Age, gender, Hgb, left ventricular hypertrophy and renal function were correlated with NT-proBNP in patients with EHT. J. Clin. Lab. Anal. 24:12,16, 2010. © 2010 Wiley-Liss, Inc. [source] Clinical value of urinary kidney biomarkers for estimation of renal impairment in elderly Chinese with essential hypertensionJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 1 2008XunHui Xu Abstract The purpose of this work was to observe the excretion of specific types of urinary proteins and urinary enzymes in elderly essential hypertension patients, for early detection and targeted treatment of hypertensive nephropathy in the elderly. A total of 120 elderly essential hypertensive patients and 38 healthy elderly volunteers were involved. The urinary excretion rate of retinal-binding protein (RBP), transferrin (Tf), albumin (Alb), and urinary enzyme N-acetyl-beta-D-glucosaminidase (NAG) activity were determined. Patients were divided into two groups according to their creatinine clearance (Cockroft-Gault formula). There were 88 patients in group A, whose glomerular filtration rate (GFR) was ,80,mL/min, and 32 patients in group B with a GFR <80,mL/min. Among the essential hypertensive patients, urinary excretion rates of RBP, Alb, Tf, and NAG were increased in both groups compared with the healthy controls. But the amount of urinary protein differed between group A and group B. The excretion rate of specific urinary protein and urinary enzyme had a positive relationship with the duration of course of hypertension. We believe that specific types of urinary proteins and urinary enzymes may be useful markers for early diagnosis of hypertensive nephropathy; they can also be regarded as a clinical indicator of the progression of hypertensive nephropathy, serving in the assessment of therapeutic effects. J. Clin. Lab. Anal. 22:86,90, 2008. © 2008 Wiley-Liss, Inc. [source] Angiotensin-converting enzyme gene insertion/deletion polymorphism frequency in normotensive children with a positive family history of essential hypertensionJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 12 2009Lale Camci Aim: To evaluate the possible relationship between blood pressure (BP) and angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in normotensive children with a positive family history of essential hypertension (EHT). Material and Methods: Three hundred seventy-six randomly selected normotensive schoolchildren (147 boys, 229 girls) between the ages of seven and 17 years were enrolled. Children were subdivided into a ,first-degree relative group' and a ,second-degree relative group' according to the presence of EHT in parents or grandparents, respectively. BP was measured twice from the right arm and the systolic BP, diastolic BP and mean BP were recorded. ACE gene I/D polymorphism was performed from all studied children and frequency od DD, ID and ID allele were analysed in each study group. Results: Allelic frequencies of the DD genotype of the ACE gene were higher in children with a positive history in the first- (36.2%) and second-degree (38.3%) relatives for EHT than the controls (30.7%) (P < 0.05 for both). Children with a positive family history of EHT and a DD genotype, had significantly higher SBP, DBP and MBP levels (P < 0.05) than the children with ID or II genotypes. Conclusion: We found that the ACE gene DD genotype was common and that BP levels were higher in Turkish children with a positive family history of EHT and DD genotype. Because the presence of DD allele might be the one of the potential contributor of EHT pathogenesis, further studies needed in large cohort for long term follow-up for EHT in children with DD allele. [source] Diagnosis And Treatment Of Hypertension In Children And AdolescentsJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 2 2003Rosalind M. Peters PhD Purpose To provide nurse practitioners (NPs) with updated information regarding the etiology, diagnosis,and treatment of childhood hypertension. Data Sources Extensive review of the scientific literature regarding hypertension, including the latest NIH recommendations. Conclusions Hypertension affects more than 350,000 American children. While the majority of hypertension in early childhood occurs from secondary causes, the incidence of essential hypertension in later childhood and adolescence is rising, raising concerns as elevated pressures in childhood "track" into adulthood. Early detection and treatment of elevated childhood pressures represent important steps in reducing long-term cardiovascular risk. Implications for Practice NPs must be able to accurately differentiate between primary and secondary hypertension in childhood. Secondary hypertension requires prompt diagnosis and treatment, and controlling primary childhood hypertension has life-long implications. Given the familial predispo-sition to hypertension, it is important for adult NPs to be aware of the risks faced by children of hypertensive patients. [source] Arterial Rigidity And Cardiovascular Sympathetic Tone In Hypertensive Obese And Type 2 Diabetic PatientsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000P Valensi An increase of arterial rigidity and sympathetic activity has been suggested to contribute to essential hypertension. We have shown that vagal control of heart rate (HR) variations during standardized tests is similarly impaired in normotensive obese and type 2 diabetic patients. The aim was to compare cardiovascular vagosympathetic balance and the link between pulse pressure, an index of arterial rigidity, and sympathetic activity in normotensive and hypertensive obese and type 2 diabetic patients. Groups 1 and 2 consisted of 70 normotensive and 32 hypertensive obese patients, groups 3 and 4 of 18 normotensive and 14 hypertensive diabetic patients respectively. HR and blood pressure (BP) variations were studied with a plethysmographic system and spectral analysis (Finapres). During a 5 min-period at a controlled breathing rate, in the 4 groups, the high frequency peak of HR variations (vagal control) was significantly lower than in controls (19 healthy subjects), and the mid/high frequency peak ratio of HR variations was significantly increased. During a standing test, the mid-frequency peak of systolic BP variations (sympathetic activity) did not differ significantly in obese or diabetic patients, either normotensive or hypertensive, and in controls. This peak correlated significantly with pulse pressure in groups 2 and 4 and in the control group but not in groups 1 and 3. In conclusion, 1) spectral analysis confirms that in obese and diabetic patients vagal control of HR variations is similarly reduced and suggests that sympathetic activity is relatively increased ; 2) in hypertensive patients sympathetic tone is not higher than in normotensive ones, but may contribute to arterial rigidity. [source] Microvascular Structure and Function in Salt-Sensitive HypertensionMICROCIRCULATION, Issue 4 2002Dr. Matthew A. Boegehold In many individuals with essential hypertension, dietary salt can further increase blood pressure by augmentation of an already elevated total peripheral resistance. There is little information on the microvascular changes that contribute to salt-sensitive hypertension in humans, but studies in the Dahl salt-sensitive rat have provided some knowledge of the microcirculation in this form of hypertension. These studies, most of which have used intravital microscopy or isolated vessel technology, are the focus of this review. The salt-induced exacerbation of hypertension in Dahl rats is due to a uniform increase in hemodynamic resistance throughout most of the peripheral vasculature. In the spinotrapezius muscle, this resistance increase is largely due to the intense constriction of proximal arterioles. The mechanisms responsible for this increased arteriolar tone include increased responsiveness to oxygen and a loss of tonic nitric oxide (NO) availability caused by reduced endothelial NO production and/or accelerated NO degradation by reactive oxygen species. Within the last decade, it has become increasingly clear that high salt intake can also lead to changes in microvascular structure and function in the absence of increased arterial pressure. This effect must also be considered when evaluating microvascular changes and their functional consequences in salt-sensitive hypertension. [source] Carotid vascular remodelling in patients with autosomal dominant polycystic kidney diseaseNEPHROLOGY, Issue 1 2009SHU RONG SUMMARY Aim: To study carotid vascular wall remodelling in patients with autosomal dominant polycystic kidney disease (ADPKD) using integrated backscatter signal (IBS) analysis. Methods: Included in the study were: 60 ADPKD patients with preserved renal function, including 32 patient with hypertension and 28 with normotension; 25 patients with essential hypertension; and 30 healthy volunteers. Carotid intima-media thickness (IMT) was measured by 2-D conventional ultrasonography. Acoustic tissue characterization of the carotid wall was assessed by IBS analysis, and the percentage of regions considered as fibromatosis was calculated in all groups. Results: Carotid IMT in hypertensive ADPKD patients (0.8 ± 0.05 vs 0.68 ± 0.02 mm, P < 0.01 and 0.8 ± 0.05 vs 0.56 ± 0.04 mm, P < 0.01 respectively) and patients with essential hypertension (0.79 ± 0.03 vs 0.68 ± 0.02 mm, P < 0.01 and 0.79 ± 0.03 vs 0.56 ± 0.0 4 mm, P < 0.01 respectively) was significantly greater than that of normotensive patients and healthy subjects. Carotid IMT in normotensive ADPKD patients was also significantly greater than that in healthy subjects (0.68 ± 0.02 vs 0.56 ± 0.04 mm, P < 0.01). Calibrated IBS (C-IBS) in hypertensive ADPKD patients was significantly greater than that in patients with essential hypertension and normotensive ADPKD patients (,21.2 ± 1.51 dB vs ,23.1 ± 1.61 dB, P < 0.05; ,21.2 ± 1.51 dB vs ,24.5 ± 1.34 dB, P < 0.01). C-IBS in normotensive ADPKD patients was significantly greater than that in healthy subjects (,24.5 ± 1.34 dB vs ,26.2 ± 1.69 dB, P < 0.01). The percentage of regions that could be considered as fibromatosis in hypertensive ADPKD patients was significantly greater than that in patients with essential hypertension and normotensive ADPKD patients (30.0% vs 22.4%, P < 0.05; 30.0% vs 17.9%, P < 0.01). The percentage of regions that could be considered as fibromatosis in normotensive ADPKD patients was significantly greater than that in healthy subjects (15.2% vs 10.3%, P < 0.01). Conclusion: Carotid remodelling occurs in the early stage of ADPKD and can be aggravated by hypertension. Fibrosis contributes to the vascular rearrangement. [source] Studies on the effects of gentamicin on rat metanephric development in vitroNEPHROLOGY, Issue 1-2 2000Luise A Cullen SUMMARY: Reduced nephron endowment has been associated with increased risk of developing essential hypertension and chronic renal failure. Both in vivo and in vitro exposure of developing rat metanephroi to gentamicin has been reported to inhibit metanephric development resulting in reduced nephron endowment. The aim of the present study was to confirm that gentamicin results in reduced nephron endowment in vitro, and to extend understanding of the mechanisms responsible for this reduced endowment. Embryonic day 14 (E14) rat metanephroi were cultured for up to 4 days in serum-free medium with or without 50 ,g/mL gentamicin. Metanephroi cultured in the presence of gentamicin were 25% smaller than control metanephroi after 2 days culture and 30% smaller after 4 days (P < 0.001). This decrease in total metanephric volume was reflected in reduced volumes of ureteric duct epithelium, mesenchyme/interstitium and nephron epithelia. The reduced volume of ureteric duct epithelium in gentamicin-treated metanephroi was associated with a 30% reduction in the number of ureteric duct branch points at 2 days. Metanephroi cultured with gentamicin contained 20% fewer glomeruli than control metanephroi (P < 0.005) at 4 days. These glomeruli were 30% smaller than control glomeruli (P < 0.05). Qualitative observations of Pax-2 immunostained mesenchymal condensates indicated no difference in condensate size, location or morphology. These results confirm that in vitro exposure of developing rat metanephroi to gentamicin results in reduced nephron endowment. The defect in nephrogenesis centres around the inhibition of ureteric duct branching. [source] Investigation of the antihypertensive effect of oral crude stevioside in patients with mild essential hypertensionPHYTOTHERAPY RESEARCH, Issue 9 2006Letícia A. F. Ferri Abstract The antihypertensive effect of crude stevioside obtained from the leaves of Stevia rebaudiana (Bertoni) Bertoni (Compositae) on previously untreated mild hypertensive patients was examined. Patients with essential hypertension were submitted to a placebo phase for 4 weeks. The volunteers selected in this phase were randomly assigned to receive either capsules containing placebo during 24 weeks or crude stevioside 3.75 mg/kg/day (7 weeks), 7.5 mg/kg/day (11 weeks) and 15.0 mg/kg/day (6 weeks). All capsules were prescribed twice a daily (b.i.d.), i.e. before lunch and before dinner. After the placebo phase and after each dose of crude stevioside, body mass index, electrocardiogram and laboratory tests were performed. During the investigation blood pressure (BP) was measured biweekly and the remaining data were collected at the end of each stevioside dose step. All adverse events were prospectively recorded but no major adverse clinical effects were observed during the trial. Systolic and diastolic BP decreased (p < 0.05) during the treatment with crude stevioside, but a similar effect was observed in the placebo group. Therefore, crude stevioside up to 15.0 mg/kg/day did not show an antihypertensive effect. Moreover, the results suggest that oral crude stevioside is safe and supports the well-established tolerability during long term use as a sweetener in Brazil. Copyright © 2006 John Wiley & Sons, Ltd. [source] Effects of essential hypertension on short latency human somatosensory-evoked potentialsPSYCHOPHYSIOLOGY, Issue 2 2010Louisa Edwards Abstract Reduced perception of somatosensory stimulation in patients with essential hypertension may be due to deficits in the ascending somatosensory pathway. Function in the ascending somatosensory pathway was assessed by measuring N9, N13, and N20 somatosensory-evoked potentials in 14 unmedicated essential hypertensives and 22 normotensives. N9 amplitudes were smaller and N13 amplitudes marginally smaller in hypertensives than normotensives. N9 amplitudes were inversely associated with blood pressure. N20 amplitudes and N9, N13, and N20 latencies did not differ between groups. In addition, plexus-to-cord, cord-to-cortex, and plexus-to-cortex conduction times were not different between groups. These data suggest that hypertension affects the peripheral nervous system by reducing the number of active sensory nerve fibers without affecting myelination. However, hypertension does not seem to affect the afferent somatosensory pathway within the brain. [source] De novo expression of Kv6.3 contributes to changes in vascular smooth muscle cell excitability in a hypertensive mice strainTHE JOURNAL OF PHYSIOLOGY, Issue 3 2009Alejandro Moreno-Domínguez Essential hypertension involves a gradual and sustained increase in total peripheral resistance, reflecting an increased vascular tone. This change associates with a depolarization of vascular myocytes, and relies on a change in the expression profile of voltage-dependent ion channels (mainly Ca2+ and K+ channels) that promotes arterial contraction. However, changes in expression and/or modulation of voltage-dependent K+ channels (Kv channels) are poorly defined, due to their large molecular diversity and their vascular bed-specific expression. Here we endeavor to characterize the molecular and functional expression of Kv channels in vascular smooth muscle cells (VSMCs) and their regulation in essential hypertension, by using VSMCs from resistance (mesenteric) or conduit (aortic) arteries obtained from a hypertensive inbred mice strain, BPH, and the corresponding normotensive strain, BPN. Real-time PCR reveals a differential distribution of Kv channel subunits in the different vascular beds as well as arterial bed-specific changes under hypertension. In mesenteric arteries, the most conspicuous change was the de novo expression of Kv6.3 (Kcng3) mRNA in hypertensive animals. The functional relevance of this change was studied by using patch-clamp techniques. VSMCs from BPH arteries were more depolarized than BPN ones, and showed significantly larger capacitance values. Moreover, Kv current density in BPH VSMCs is decreased mainly due to the diminished contribution of the Kv2 component. The kinetic and pharmacological profile of Kv2 currents suggests that the expression of Kv6.3 could contribute to the natural development of hypertension. [source] Human Chromosome 17 in Essential HypertensionANNALS OF HUMAN GENETICS, Issue 2 2003J. Knight Summary Hypertension affects up to 30% of the adult population in Western societies and is a major risk factor for kidney disease, stroke and coronary heart disease. It is a complex trait thought to be influenced by a number of genes and environmental factors, although the precise aetiology remains unknown at this time. A number of methods have been successfully used to identify mutations that cause Mendelian traits and these are now being applied to the investigation of complex diseases. This review summarises the data gathered, using such approaches, that suggest there is a gene or genes on chromosome 17 causing human essential hypertension. Studies in rodent models are discussed first, followed by studies of human hypertension that include the investigation of pseudohypoaldosteronism type II, a monogenic trait that manifests with hypertension alongside other phenotypic variables. In addition, candidate gene studies, genome screens and linkage studies based on comparative mapping are outlined. To date no gene has been identified on human chromosome 17 that influences blood pressure and causes human essential hypertension. However, results of ongoing fine mapping and candidate gene studies in both rodents and man are eagerly awaited. [source] Association of a polymorphism at the 5,-region of the angiotensin II type 1 receptor with hypertensionANNALS OF HUMAN GENETICS, Issue 3 2000N. TAKAHASHI Molecular variants of individual components of the renin-angiotensin system are thought to contribute to inherited predisposition towards essential hypertension. Using polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) and sequence analysis, we identified seven polymorphisms in the 5,-flanking region of the angiotensin II type 1 receptor (AGTR1/AT1) gene. We conducted a case-control study in a sample from the Japanese population to determine whether polymorphic markers in the 5,-flanking region of the AT1gene were associated with essential hypertension. The study compared 149 hypertensive subjects to 156 normotensive control subjects. A significantly higher frequency of the AT1(,535)*T allele was observed in hypertensive subjects. Evidence was obtained that the AT1(,535)*T allele showed a synergistic effect on risk of hypertension with angiotensin I converting enzyme D allele (ACE*D). [source] Recombinant human relaxin in the treatment of systemic sclerosis with diffuse cutaneous involvement: A randomized, double-blind, placebo-controlled trial,ARTHRITIS & RHEUMATISM, Issue 4 2009Dinesh Khanna Objective A phase II randomized controlled trial of recombinant human relaxin suggested that a dosage of 25 ,g/kg/day was safe and clinically effective in improving skin disease and reducing functional disability in scleroderma (systemic sclerosis; SSc). We undertook a large randomized, double-blind, placebo-controlled clinical trial to compare placebo with 10 ,g/kg/day and 25 ,g/kg/day recombinant human relaxin, given for 24 weeks in patients with stable, diffuse, moderate-to-severe SSc. Methods Men and women ages 18,70 years with diffuse cutaneous SSc (dcSSc) were administered recombinant human relaxin (10 ,g/kg/day or 25 ,g/kg/day) or placebo for 24 weeks as a continuous subcutaneous infusion. There was a followup safety visit at week 28. Results The primary outcome measure, the modified Rodnan skin thickness score, was similar among the 3 groups at baseline and at weeks 4, 12, and 24. Secondary outcomes such as functional disability were similar in all 3 groups, while the forced vital capacity decreased significantly in the relaxin groups. The discontinuation of both doses of relaxin at week 24 led to statistically significant declines in creatinine clearance and serious renal adverse events (defined as doubling of serum creatinine, renal crisis, or grade 3 or 4 essential hypertension) in 7 patients who had received relaxin therapy but in none who had received placebo. Conclusion Recombinant relaxin was not significantly better than placebo in improving the total skin score or pulmonary function or in reducing functional disability in patients with dcSSc. In addition, relaxin was associated with serious renal adverse events, the majority of which occurred after stopping the infusion. If relaxin is used therapeutically for any conditions other than scleroderma, close monitoring of blood pressure and renal function must be performed. [source] Can we predict recurrence of pre-eclampsia or gestational hypertension?BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 8 2007MA Brown Objective, To estimate the rates of recurrence of pre-eclampsia or gestational hypertension in a subsequent pregnancy and to determine factors predictive of recurrence. Design, Retrospective cohort study. Setting, St George Public and Private Hospitals, teaching hospitals without neonatal intensive care units. Participants, A total of 1515 women with a diagnosis of pre-eclampsia or gestational hypertension between 1988 and 1998 were identified from the St George Hypertension in Pregnancy database, a system designed initially for ensuring quality outcomes of hypertensive pregnancies. Of these, 1354 women were followed up, and a further 333 records from women coded as having a normal pregnancy during that period were selected randomly as controls. Main outcome measures, Likelihood of recurrent pre-eclampsia or gestational hypertension and clinical and routine laboratory factors in the index pregnancy predictive of recurrence of pre-eclampsia or gestational hypertension. Methods, The index cases from our unit's database were linked to the matched pregnancy on the State Department of Health database, allowing us to determine whether further pregnancies had occurred at any hospital in the State. The outcome of these pregnancies was determined by review of medical records, using strict criteria for diagnosis of pre-eclampsia or gestational hypertension. Results, Almost all women with a normal index pregnancy had a further normotensive pregnancy. One in 50 women hypertensive in their index pregnancy had developed essential hypertension by the time of their next pregnancy. Women with pre-eclampsia in their index pregnancy were equally likely to develop either pre-eclampsia or gestational hypertension (approximately 14% each), while women with gestational hypertension were more likely to develop gestational hypertension (26%) rather than pre-eclampsia (6%) in their next pregnancy. Multiparous women with gestational hypertension were more likely than primiparous women to develop pre-eclampsia (11 versus 4%) or gestational hypertension (45 versus 22%) in their next pregnancy. Early gestation at diagnosis in the index pregnancy, multiparity, uric acid levels in the index pregnancy and booking blood pressure parameters in the next pregnancy significantly influenced the likelihood of recurrence, predominantly for gestational hypertension and less so for pre-eclampsia. No value for these parameters was significant enough to be clinically useful as a discriminate value predictive of recurrent pre-eclampsia or gestational hypertension. Conclusions, Approximately 70% of women with pre-eclampsia or gestational hypertension will have a normotensive next pregnancy. The highest risk group for recurrent hypertension in pregnancy in this study was multiparous women with gestational hypertension. No readily available clinical or laboratory factor in the index pregnancy reliably predicts recurrence of pre-eclampsia. [source] | |||||||||||||||||||||||||||||||