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At least 19 recordsLinked to original sources
PubMed2006

[Is essential hypertension essentially metabolic?].

Hypertension is one of the most prevalent cardiovascular risk factors. Most of the cases are not due to secondary causes and are diagnosed as essential hypertension, although a common physiopathologic link underlies for diabetes and dyslipidemia that are usually present. Most hypertensive patients have also obesity and insulin resistance and this may be more than an epidemiologic association, but one of the main physiopathologic basis of essential hypertension.

Humans↗
PubMed1992

[24-hour blood pressure changes in elderly people with isolated systolic hypertension, essential hypertension and normotension].

In order to evaluate circadian blood-pressure (BP) profile characteristics typical of old age, we compared circadian BP profile in elderly subjects with isolated systolic hypertension (ISH; greater than 160/less than 90 mmHg), essential hypertension (EH; diastolic BP greater than or equal to 95 mmHg), and normotension (N; less than 140/less than 90 mmHg). Each group consisted of 18 subjects, approximately matched in age and sex, (age range 60-82 years; mean age 67.5 years). Ambulatory 24-h BP-monitoring was carried out using a SpaceLabs 90202 with measurements made every 30 min. In ISH, causal systolic BP is higher and circadian systolic BP is lower than in EH (n.s.). Circadian diastolic BP is lower than in EH and higher than in N; both are statistically highly significant (p less than 0.001, u-test, Wilcoxon). The decrease during the resting period is 6 mmHg in EH and 17 mmHg in ISH. In ISH there is a considerable difference of 39 mmHg between casual BP and circadian 24-h BP, in contrast to N and to EH, and this is due to a particular hyperreactivity. This discrepancy is typical of old age and holds the danger of over-treatment, if only causal BP is taken into consideration.

Aged↗
PubMed1980

[Disturbance of intracellular calcium distribution in fatty tissue in hypertension (essential hypertension)].

The authors used the method of isotope exchange (45Ca) to study in vitro the distribution of calcium in the adipose tissue of the greater omentum in individuals with essential hypertension and in persons with normal arterial pressure who underwent opration mostly for chronic cholecystitis. Three pools of exchangeable calcium were revealed in the adipose tissue. The calcium content in two intracellular pools in the adipose tissue of patients with hypertension was increased respectively by 71 and 83% as compared to that in patients with normal arterial pressure.

Adipose Tissue↗
PubMed1998

Endothelial nitric oxide synthase gene is positively associated with essential hypertension.

Essential hypertension has a genetic basis. Accumulating evidence, including findings of elevation of arterial blood pressure in mice lacking the endothelial nitric oxide synthase (eNOS) gene, strongly suggests that alteration in NO metabolism is implicated in hypertension. There are, however, no reports indicating that polymorphism in the eNOS gene is associated with essential hypertension. We have identified a missense variant, Glu298Asp, in exon 7 of the eNOS gene and demonstrated that it is associated with both coronary spastic angina and myocardial infarction. To explore the genetic involvement of the eNOS gene in essential hypertension, we examined the possible association between essential hypertension and several polymorphisms including the Glu298Asp variant, variable number tandem repeats in intron 4 (eNOS4b/4a), and two polymorphisms in introns 18 and 23. We performed a large-scale study of genetic association using two independent populations from Kyoto (n=458; 240 normotensive versus 218 hypertensive subjects) and Kumamoto (n=421; 223 normotensive versus 187 hypertensive subjects), Japan. In both groups, a new coding variant, Glu298Asp, showed a strong association with essential hypertension (Kyoto: odds ratio, 2.3 [95% confidence interval, 1.4 to 3.9]; Kumamoto: odds ratio, 2.4 [95% confidence interval, 1.4 to 4.0]). The allele frequencies of 298Asp in hypertensive subjects were significantly higher than those in normotensive subjects in both groups (Kyoto: 0.103 versus 0.050, P<0.0017; Kumamoto: 0.120 versus 0.058, P<0.0013, respectively). No such disequilibrium between genotypes was significantly associated with any other polymorphisms we examined; the Glu298Asp variant was also not linked to any other polymorphisms. In conclusion, the Glu298Asp missense variant was significantly associated with essential hypertension, which suggests that it is a genetic susceptibility factor for essential hypertension.

Adult↗
PubMed1996

[Restriction fragment length polymorphism of human renin gene in essential hypertension].

Essential hypertension is a heterogenous multifactorial disease resulting from an interaction between genetic and environmental factors. Nature of genes responsible for the blood pressure regulation is not completely understood. Data from molecular biology studies with animals indicate that renin gene is involved in the pathogenesis of hypertension. Renin gene is one of the major candidate genes contributing to the pathogenesis of essential hypertension in humans. The aim of this study was the assessment of the association of RFLPs of human renin gene with essential hypertension in Polish population and search for the genetic marker of susceptibility to the disease. MspI, HindIII and EcoT141 RFLP in human renin gene locus were studied and polymorphic allele and genotype frequencies in the population of 74 hypertensive and 60 normotensive subjects were compared. MspI and HindIII RFLP analysis has not shown any statistically significant differences in allele and genotype frequencies between hypertensives and normotensives. These RFLPs do not seem to be in association with essential hypertension in studied population. EcoT141 RFLP analysis has not shown statistically significant differences in polymorphic alleles frequencies between examined groups. However, the observed difference between genotype E2O frequencies in hypertensives (0.31) and normotensives (0.12) was statistically significant (p < 0.045). A clinical importance of this finding is not known but genotype E2O seems to be a potential marker of susceptibility to essential hypertension. Further investigations in larger group of patients are required.

Gene Frequency↗
PubMed2001

Interaction of alpha(1)-Na,K-ATPase and Na,K,2Cl-cotransporter genes in human essential hypertension.

Essential hypertension is a common disease the genetic determinants of which have been difficult to unravel because of its clinical heterogeneity and complex, multifactorial, polygenic etiology. Based on our observations that alpha(1)-Na,K-ATPase (ATP1A1) and renal-specific, bumetanide-sensitive Na,K,2Cl-cotransporter (NKCC2) genes interactively increase susceptibility to hypertension in the Dahl salt-sensitive hypertensive (Dahl S) rat model, we investigated whether parallel molecular genetic mechanisms might exist in human essential hypertension in a relatively genetic homogeneous cohort in northern Sardinia. Putative ATP1A1-NKCC2 gene interaction was tested by comparing hypertensive patients (blood pressure [BP] >165/95 mm Hg) with normotensive controls age >60 years with BP <140/85 mm Hg. Genotype analysis with microsatellite markers revealed conformation to Hardy-Weinberg proportions for 6 alleles of both ATP1A1 (D1S453) and NKCC2 (NKCGT7) markers, respectively. Two-by-six chi(2) analysis of alleles identified overrepresentation of ATP1A1 No. 4 and NKCC2 No. 4 alleles, respectively, in hypertensives compared with controls. With a qualitative trait framework, single-gene analysis detected association of both the ATP1A1 No. 4 allele (P=0.004, chi(2)=8.094, df=1) and the NKCC2 No. 4 allele (P=0.0002, chi(2)=14.279, df=1) with moderate to severe hypertension. Digenic analysis revealed that ATP1A1 No. 4-NKCC2 No. 4 allele interaction increases susceptibility to hypertension (P<0.0001, chi(2)=22.3, df=1) beyond levels obtained in single-gene analysis. Analysis was also performed in a quantitative trait framework with BP as the continuous trait parameter. Digenic analysis of ATP1A1 No. 4-NKCC2 No. 4 allele interaction revealed significant association with systolic (1-way ANOVA, P=0.000076) and diastolic (P=0.00099) BP. Interaction was corroborated by 2x2 factorial ANOVA for interaction (systolic BP interaction term, P<0.05, diastolic BP interaction term, P=0.035). The data are compelling that ATP1A1 and NKCC2 genes are candidate interacting hypertension-susceptibility loci in human essential hypertension and affirm gene interaction as an important genetic mechanism underlying hypertension susceptibility. Although corroboration in other cohorts and identification of functionally significant mutations are imperative next steps, the data provide a genotype-stratification scheme, with 4-fold predictive value (odds ratio, 4.28; 95% confidence interval, 2.29 to 8.0), which could help decipher the complex genetics of essential hypertension.

Adult↗
PubMedDate not supplied

The pathogenesis of essential hypertension.

Essential hypertension is a quantitative abnormality, the pathological effects and risks increasing with the blood pressure level. In Western countries blood pressure rises with age in most individuals, so essential hypertension is more frequent in middle and older age groups. It is likely that an individual's blood pressure level is determined by many interacting factors. These include heredity, which probably acts multifactorially, and many environment influences, including psychological stress and obesity. Specific factors may be of varying importance in different individuals and in different populations. Several physiological mechanisms control the blood pressure level and may be altered in essential hypertension. In early hypertension sympathetic nervous activity is sometimes increased, although in long-standing hypertension this is less marked. Cardiac output may be increased in borderline hypertension but is normal in established hypertension, when total peripheral resistance is increased. Total exchangeable sodium is normal, while the renal pressure-natriuresis balance is altered, so that for a given pressure the hypertension kidney excretes less sodium. In some patients, plasma renin is low, probably as a result of renal adaption to prolonged hypertension. The pathogenic sequence in essential hypertension is uncertain. Increased autonomic activity may cause vasoconstriction in renal and other arterioles and increase cardiac output, leading to a rise in blood pressure. Elevated pressure itself produces structural changes in the resistance vessels, including those of the kidney, which eventually maintain the hypertension even when the initiating stimulus is removed. The way in which heredity and environment influence pathogenic mechanism is also uncertain. Heredity might, for example, influence the autonomic response to stress or the liability to irreversible changes in the resistance vessels or in the kidney. Environmental factors may also increase autonomic activity, enhance vascular reactivity or alter renal function.

Blood Pressure↗
PubMed1995

Insulin action on heart and skeletal muscle glucose uptake in essential hypertension.

Essential hypertension is characterized by skeletal muscle insulin resistance but it is unknown whether insulin resistance also affects heart glucose uptake. We quantitated whole body (euglycemic insulin clamp) and heart and skeletal muscle (positron emission tomography and 18F-fluoro-2-deoxy-D-glucose) glucose uptake rates in 10 mild essential hypertensive (age 33 +/- 1 yr, body mass index 23.7 +/- 0.8 kg/m2, blood pressure 146 +/- 3/97 +/- 3 mmHg, VO2max 37 +/- 3 ml/kg per min) and 14 normal subjects (29 +/- 2 yr, 22.5 +/- 0.5 kg/m2, 118 +/- 4/69 +/- 3 mmHg, 43 +/- 2 ml/kg per min). Left ventricular mass was similar in the hypertensive (155 +/- 15 g) and the normotensive (164 +/- 13 g) subjects. In the hypertensives, both whole body (28 +/- 3 vs 44 +/- 3 mumol/kg per min, P < 0.01) and femoral (64 +/- 11 vs 94 +/- 8 mumol/kg muscle per min, P < 0.05) glucose uptake rates were decreased compared to the controls. In contrast, heart glucose uptake was 33% increased in the hypertensives (939 +/- 51 vs 707 +/- 46 mumol/kg muscle per min, P < 0.005), and correlated with systolic blood pressure (r = 0.66, P < 0.001) and the minute work index (r = 0.48, P < 0.05). We conclude that insulin-stimulated glucose uptake is decreased in skeletal muscle but increased in proportion to cardiac work in essential hypertension. The increase in heart glucose uptake in mild essential hypertensives with a normal left ventricular mass may reflect increased oxygen consumption and represent an early signal which precedes the development of left ventricular hypertrophy.

Adult↗
PubMed2003

Clinical trial of extended-release felodipine in pediatric essential hypertension.

Essential hypertension in pediatric patients may require pharmacological treatment. There is a need for efficacious, safe, and well-tolerated antihypertensive agents with a once-a-day dosing regimen in children and adolescents. The aim of the trial was to evaluate the dose-response and tolerability of the dihydropyridine calcium channel blocker, felodipine extended-release tablets (felodipine ER), given once daily to pediatric patients with essential hypertension. A randomized double-blind, parallel-group, multi-center clinical study comparing felodipine ER (2.5, 5, or 10 mg once daily) and placebo was performed on pediatric patients with a baseline systolic (SBP) or diastolic blood pressure (DBP) above the 95th percentile for age, sex, and height. Of 133 randomized patients, 128 (96.2%) completed the 3 weeks of double-blind treatment. The study population included 50% children 6-12 years of age or Tanner stage <or=3, 39% black, and 40% female patients. All doses of felodipine ER and placebo decreased both SBP and DBP. The 5-mg dose of felodipine ER resulted in a significant decline in trough sitting, standing, and supine DBP (placebo-adjusted, -4.6, -5.06, and -5.05 mmHg, respectively, P<0.05) compared with placebo. However, there was no significant decline in SBP. The 2.5- and 10-mg doses showed no significant differences compared with placebo in lowering BP. The effect of felodipine ER was comparable in patient subgroups by age, race, and gender. The drug was well tolerated. The study failed to show a dose response of felodipine ER in pediatric patients with essential hypertension. This finding might be explained in part by the limitations of study design. The spectrum of side effects in pediatric patients was comparable with that in adults, except for a lower incidence of peripheral edema. Further studies are needed to clarify the role of felodipine ER in the management of children and adolescents with essential hypertension.

Adolescent↗
PubMed2002

G protein-coupled receptor kinase 4 gene variants in human essential hypertension.

Essential hypertension has a heritability as high as 30-50%, but its genetic cause(s) has not been determined despite intensive investigation. The renal dopaminergic system exerts a pivotal role in maintaining fluid and electrolyte balance and participates in the pathogenesis of genetic hypertension. In genetic hypertension, the ability of dopamine and D(1)-like agonists to increase urinary sodium excretion is impaired. A defective coupling between the D(1) dopamine receptor and the G protein/effector enzyme complex in the proximal tubule of the kidney is the cause of the impaired renal dopaminergic action in genetic rodent and human essential hypertension. We now report that, in human essential hypertension, single nucleotide polymorphisms of a G protein-coupled receptor kinase, GRK4gamma, increase G protein-coupled receptor kinase (GRK) activity and cause the serine phosphorylation and uncoupling of the D(1) receptor from its G protein/effector enzyme complex in the renal proximal tubule and in transfected Chinese hamster ovary cells. Moreover, expressing GRK4gammaA142V but not the wild-type gene in transgenic mice produces hypertension and impairs the diuretic and natriuretic but not the hypotensive effects of D(1)-like agonist stimulation. These findings provide a mechanism for the D(1) receptor coupling defect in the kidney and may explain the inability of the kidney to properly excrete sodium in genetic hypertension.

Animals↗
PubMed2001

The genetics of essential hypertension.

Essential hypertension is an escalating problem for industrialized populations. It is currently seen as a 'complex' genetic trait caused by multiple susceptibility genes the effects of which are modulated by gene-environment and gene-gene interactions. Nevertheless, the success to date in identifying these susceptibility genes has been very limited. A number of candidates has been proposed, but demonstrating consistently the linkage or association with hypertension has been problematic. The data for angiotensinogen is undoubtedly the most extensive and meta-analysis has confirmed a significant association overall, although the risk contributed by this gene appears to be modest (odds ratio of 1.2). Identifying further genes - probably conferring even smaller attributable risks - represents a major challenge for future developments in this area. This contrasts markedly with the success that has been achieved in the past 5 years in solving the molecular genetics of a number of rare familial hypertension syndromes. The true incidences of some of these disorders may be higher than first appreciated, but it is still unclear if the genes for these syndromes also play a part in essential hypertension. A more complete understanding of the genetic basis of essential hypertension should be possible in the coming years using new strategies that take advantage of the information provided by the human genome project. This knowledge will irrevocably change the way we approach this disease in terms of its diagnosis, risk assessment for end-points such as stroke and heart disease, and the customised treatment that might be offered in the future.

Animals↗
PubMed1991

Association and linkage analyses of restriction fragment length polymorphisms for the human renin and antithrombin III genes in essential hypertension.

Essential hypertension is a highly hereditable disorder in which genetic influences predominate over environmental factors. The molecular genetic profiles which predispose to essential hypertension are not known. In rats with genetic hypertension, there is some recent evidence pointing to linkage of renin gene alleles with blood pressure. The genes for renin and antithrombin III belong to a conserved synteny group which, in humans, spans the q21.3-32.3 region of chromosome I and, in rats, is linkage group X on chromosome 13. The present study examined the association of particular human renin gene (REN) and antithrombin III gene (AT3) polymorphisms with essential hypertension by comparing the frequency of specific alleles for each of these genes in 50 hypertensive offspring of hypertensive parents and 91 normotensive offspring of normotensive parents. In addition, linkage relationships were examined in hypertensive pedigrees with multiple affected individuals. Alleles of a REN HindIII restriction fragment length polymorphism (RFLP) were detected using a genomic clone, lambda HR5, to probe Southern blots of HindIII-cut leucocyte DNA, and those for an AT3 PstI RFLP were detected by phATIII 113 complementary DNA probe. The frequencies of each REN allele in the hypertensive group were 0.76 and 0.24 compared with 0.74 and 0.26 in the normotensive group. For AT3, hypertensive allele frequencies were 0.49 and 0.51 compared with normotensive values of 0.54 and 0.46. These differences were not significant by chi 2 analysis (P greater than 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

[Role of the angiotensinogen gene for essential hypertension].

Essential hypertension is a complex disease influenced by different genetic and environmental factors. The renin-angiotensin system (RAS) is implicated in blood pressure regulation. Angiotensinogen (AGT) is the precursor of the biologically active angiotensin II (Ang II). Initial studies on hypertensive siblings and case-control studies indicated the important role of the angiotensinogen gene (AGT) for the predisposition to essential hypertension, preeclampsia and obesity-related hypertension. Recently, different AGT polymorphisms had been identified and analyzed in case-control studies. The aim of present studies is the analysis of potentially functional AGT variants (C-532T, G-6A), which might be responsible for the regulation of gene expression and therefore AGT generation. The A-6 allele is in complete linkage disequilibrium with the T235 allele and is associated with higher AGT expression in vitro. Segregation linkage analysis demonstrated that the C-532T polymorphism influences plasma AGT variability more significantly than the G-6A variant. Since the C-532T polymorphism is located within a AP-2 consensus element, functional promoter analyses are required. The understanding of the molecular basis of RAS in essential hypertension may provide us with new and more specific pharmacological agents and perhaps the ability to individualize antihypertensive treatment.

Alleles↗
PubMed2000

Correlative factors of insulin resistance in essential hypertension.

Essential Hypertension (EH) is correlated with a metabolic disturbance characterized by insulin resistance (IR). In this study, there were observed in 47 subjects with EH and 30 subjects with normal blood pressure. Serum levels of insulin-like growth factor-1 (IGF-1), serum levels of growth hormone (GH), the activity of erythrocyte insulin receptors (EIR), and ATP levels in erythrocytes, the insulin sensitivity index (ISI) was used to study the correlative factors of essential hypertension. 1. Among patients with EH, ISI, GH, and low-affinity insulin binding sites of EIRs (RT2) were found to be in significantly lower amounts, IGF-1 levels and the KD2 of the erythrocyte insulin receptors were noted to be significantly higher. Compared with the control group, there was a marked difference between EH group and the control group. However, no statistical difference was observed between the hypertensive group and the group with normal blood pressure as regards erythrocyte ATP levels, high-affinity insulin binding sites of EIRs (RT1), and the KD1 of EIRs. 2. In the hypertensive group, the ISI was negatively correlated with mean arterial blood pressure (MBP), a family history of hypertension, the body mass index (BMI), the waist-hip ratio (WHR) and IGF-1 levels (r=-0.614delta, -0.354**, -0.386**, -0.472**, -0.298*, delta p < 0.001, **p < 0.01, *p < 0.05), were positively correlated with RT2 and GH levels (r=0.301**, 0.275*, **p < 0.01, *p < 0.05). There were no statistically significant differences between ISI and age, sex, smoking history, drinking, RT1, KD1, and ATP levels in erythrocytes. 3. The ISI was used as the dependent variable in multiple linear stepwise regression analysis. MBP (X1), a family history of EH (X2), WHR (X3), GH (X4), IGF-1 (X5), RT2 (X6), and the body mass index (X7) was used as independent variables. X1, X2, X3, X5, X6, and X7 were used in the equations. The results indicate that patients with EH also tend to have IR. We suggest that MBP, a family history of hypertension, BMI, WHR, IGF-1, and RT2 might be independent factors affecting IR in cases of essential hypertension.

Adenosine Triphosphate↗