Essential Hypertensive Individuals Research Articles

Vitamin D receptor gene polymorphisms and plasma renin activity in essential hypertensive individuals.

Several studies analyzed 25-hydroxyvitamin D (25[OH]D) and blood pressure (BP) relationship with mixed results. Moreover, a relationship between the risk of hypertension and vitamin D receptor (VDR) gene polymorphisms, FokI and BsmI, was reported. This study was aimed to analyze these relationships in essential hypertensive (EH) patients. Seventy-one EH patients, 18-75 years old, were enrolled. Patients underwent clinical BP, 24-h ambulatory BP monitoring, 25[OH]D and plasma renin activity (PRA) evaluations. FokI and BsmI VDR polymorphisms were analyzed and compared with those of 72 healthy controls. In EH patients, the median 25[OH]D levels were lower than 30 ng ml(-1). We found a significant negative correlation between 25[OH]D and 24-h systolic BP (r = -0.277, P = 0.043). This correlation persisted in backward stepwise multivariate analyses (β = -0.337; P = 0.022), after adjustment for age, gender, body mass index, glomerular filtration rate, and PRA. We did not observe statistically significant correlation between 25[OH]D and PRA. We compared the allelic frequencies and genotype distribution between patients and controls, and FokI and BsmI VDR polymorphisms were not associated either with hypertensive status or with PRA. Further wide studies are needed to clarify this relationship.

Assessment of primary healthcare professionals’ management of hypertensive patients with riser pattern

Ambulatory blood pressure monitoring (ABPM) was implemented in our primary care setting four years ago. Since then, 450 ABPMs have been performed and 69 riser subjects identified. The riser pattern is an independent risk factor for both incidence of cardiovascular events and their associated mortality. The purpose of this study was to assess the amount of control of essential hypertension (EH) among riser patients and to evaluate how our health professionals manage therapeutic changes in riser individuals. This retrospective study involved 34,289 inhabitants served in a centre in the Barcelona metropolitan area. EH individuals (450) were recruited and ABPM was performed following guidelines of the MAPAPRES (www.cardiorisc.com/MP/index_MP.asp). Good control of blood pressure was observed in 46% of dipper and non-dipper subjects but only 35% of riser subjects had blood pressures within good control ranges. The measured cardiovascular risk was either high or very high in 35% of riser individuals. Changes in medication were introduced in riser patients with both good and poor blood pressure control. A second follow-up ABPM was done in only 27% of the riser individuals. In these subjects, therapeutic changes successfully modified ABPM patterns in 87% of cases. Therapeutic changes in riser patients were introduced when these subjects were poorly controlled and these changes were highly effective. Additional ABPM to confirm the effectiveness of therapeutic changes was only performed in some individuals. Thus, for management of riser patients, more specific training of health professionals is needed.

Increased platelet activation and inflammatory response in patients with masked hypertension

Masked hypertension is associated with an increase in cardiovascular risk. Mean platelet volume (MPV), a determinant of platelet function, is a new risk factor for atherothrombosis. High-sensitive C-reactive protein (CRP) is an exquisitely sensitive systemic marker of inflammatory response. We designed this study to evaluate MPV and CRP in masked hypertensive patients and to compare those with essential hypertensive and healthy normotensive individuals. Forty-two untreated masked hypertensive patients, 53 untreated essential hypertensive patients and age-sex matched 37 normotensive healthy individuals were included in the study. Blood samples were collected and haematological parameters were measured. Plasma CRP level was measured by immunonephelometery method. The MPV was significantly higher in masked hypertensive (8.8 ± 1.6 fl) and essential hypertensive patients (9.1 ± 1.7 fl) than those of normotensive control individuals (7.8 ± 0.8 fl) (P = 0.01 and P = 0.003, respectively), whereas there was no significant difference between the masked hypertensive and essential hypertensive individuals (P > 0.05). CRP levels were also significantly higher in masked hypertensive patients than in normotensives individuals (3.31 ± 1.70, 1.98 ± 1.56 mg/l, P < 0.001, respectively). There was a significant positive correlation between MPV and CRP levels (P < 0.001, r = 0.850) in masked hypertensive patients. Patients with masked hypertension have higher MPV and CRP values than controls. Increased MPV and CRP levels may be the possible mechanisms behind the increased cardiovascular risk in masked hypertensive patients.

The Association Study of PRKG1 Gene Polymorphism and Salt-Sensitive Hypertension among the Essential Hypertension in Beijing

Background: PRKG1 plays an important role in regulating vascular smooth muscle contraction. And this gene is regarded as one of the candidate genes on salt-sensitive hypertension. The aim of this study was to investigate the effects of environmental risk factors and two SNPs and haplotypes structures of PRKG1 gene with blood salt-sensitive patients among essential hypertension. Method: Three hundred and forty-two essential hypertensive were recruited in a case-case study, a modified Sullivan’s acute salt load method was conducted to identify the salt-sensitivity and salt-resistant. Medical history and lifestyle risk factors were obtained by questionnaire, and blood and urine specimens were collected to test the biochemical indicators. We used the Sequenom Mass ARRAY Platform for genotyping of PRKG1 gene single nucleotide polymorphisms (SNPs) (rs7897633/SNP1, rs1904694/SNP2). We applied statistical software SPSS17.0, multifactor dimensionality reduction method 1.1.0 and haploview 4.0 to do the analyses. Results: There were 63 salt sensitivity subjects in 342 essential hypertension individuals, accounting for 18.4% of the total. Age and 24-hour urinary sodium concentration were the risk factors associated with salt-sensitive hypertension. The results of the logistic regression model showed that subjects carrying SNP1-AA genotype and SNP2-GG genotypes had 2.83-fold (95% CI: 1.21-6.63) and 3.50-fold (95% CI: 1.54-7.93) risks to have salt-sensitive hypertension, respectively. Haplotype analysis showed that haplotype CA had 0.56-fold (95% CI: 0.38-0.84) decreased risk for salt-sensitive hypertension, whereas, haplotype AG had 1.78-fold (95% CI: 1.20-2.65) increased risk for saltsensitive hypertension. Conclusion: Age and 24-hour urinary sodium concentration are the environmental risk factors associated with salt-sensitive hypertension. Genotypes of SNP1-AA, SNP2-GG and haplotype AG of PRKG1 gene were risk factors for salt-sensitivity in essential hypertension.

Management approaches to hypertension in autonomic failure

Supine hypertension is a common finding in autonomic failure that can worsen orthostatic hypotension and predispose to end-organ damage. This review focuses on nonpharmacologic and pharmacologic approaches to manage hypertension in these patients in the face of disabling orthostatic hypotension. The hypertension of autonomic failure can be driven by sympathetic-dependent or independent mechanisms, contingent on the site of autonomic lesions. Management of supine hypertension should include simple nonpharmacologic approaches including avoiding the supine position during the daytime and sleeping in a head-up tilt position at night. Most patients, however, require pharmacologic treatment. Several antihypertensive therapies lower nighttime pressure in autonomic failure, but none improve nocturnal volume depletion or morning orthostatic tolerance. Regardless, treatment may still be beneficial in some patients but must be decided on an individual basis. Blood pressure monitoring is helpful in this regard, as well as titration of doses, as these patients are hypersensitive to depressor agents due to loss of baroreceptor reflexes. Autonomic failure provides a unique opportunity to study blood pressure regulation independent of autonomic influences. Understanding mechanisms driving supine hypertension will have important implications for the treatment of autonomic failure and will improve our knowledge of cardiovascular regulation in other populations, including essential hypertension and elderly hypertensive individuals with comorbid orthostatic hypotension.

The adenosine system in skeletal muscle of individuals with essential hypertension and the effect of physical training

The study examined vascular function and the adenosine (ADO) system in skeletal muscle of individuals diagnosed with essential hypertension (EH; N=10) and normotensive (N; N=11) individuals, before and after a period of aerobic training. Before and after the training period, the subjects participated in two experiments in which a) leg blood flow was determined during arterial infusion of ADO, acetylcholine (ACh) or during exercise, and b) interstitial fluid was sampled from v. lateralis muscle during exercise and ADO infusion. Leg vascular conductance (LVC) in response to arterial ADO infusion was similar in the EH and N group. Interstitial ADO formation during exercise was lower in the EH than the N group. In EH, the period of training did not affect vasodilator responsiveness to arterially infused ADO but improved the formation of interstitial ADO and prostacyclin. In the N group, training resulted in a lower LVC in response to arterial ADO infusion, which was paralleled by a lower leg blood flow during submaximal exercise. In conclusion, whereas the responsiveness to circulating ADO in individuals with essential hypertension remained unaltered with training, the capacity to form ADO and prostacyclin at the microcirculatory level was enhanced, suggesting an improvement in microvascular blood flow regulation. In normotensive individuals, aerobic training reduced the vasodilatory response to intraluminal ADO.

HSG/Mfn2 Gene Polymorphism and Essential Hypertension: a Case-Control Association Study in Chinese

Hyperplasia suppressor gene/mitofusion-2 (HSG/Mfn2) is a hyperplasia suppressor gene and an essential component of mitochondrial fusion machinery; however, the association between the single nucleotide polymorphism (SNP) of HSG/Mfn2 and hypertension is unclear. In this study, 542 normotensive subjects (NT group) and 539 hypertensive patients (EH group) were screened for an association study between HSG/Mfn2 and hypertension. The results showed that the genotype distribution and allelic frequency of rs873457, rs2336384, rs1474868, rs4846085 and rs2236055 were significantly different (p lt; 0.05 for all) between EH and NT groups, although those of rs4240897 and rs873458 were not. When comparing the dominant model, significant differences still existed (p lt; 0.05 for all). The allelic frequency of rs4240897 was also slightly different between EH and NT groups (P = 0.047). When subgrouped by sex, the genotype distribution and allelic frequency of all the SNPs (except rs873458) were significantly different in male (p lt; 0.05 for all) but not in female groups. For all the SNPs, only the allelic frequency of rs4240897 was obviously different in female NT and EH groups (p lt; 0.01). Logistic regression showed that body mass index and rs873457 were closely associated with BP after adjusting for age. The frequency of the C-G-A-A-A-C-C haplotype was significantly higher in essential hypertensive patients versus control individuals, both in the entire population, in male or female groups (p lt; 0.01 for all). As for other haplotypes, most were only significantly different in the entire population and male subjects. The genetic variations of HSG/Mfn2 may be associated with hypertension in male Chinese.

Adipokines and Cardiometabolic Profile in Primary Hyperaldosteronism

Primary aldosteronism (PA) has been recently associated with an unfavorable cardiometabolic profile. However, whether pro- and antiinflammatory adipokines levels can vary in PA is unknown. We evaluated the circulating levels of resistin, leptin, and adiponectin, echocardiographic left ventricle (LV) parameters, and the prevalence of metabolic syndrome (SM) in subjects with PA. Seventy-five subjects with established diagnosis of PA and 232 consecutive individuals with known or suspected hypertension were enrolled. Plasma adipokine levels and echocardiographic parameters were calculated. Prevalence of SM was also estimated. Among the 75 PA subjects, 37 patients were affected by aldosterone-producing adenoma and 38 by idiopathic hyperaldosteronism; 40 subjects were affected by essential hypertension (EH) and SM (EH SM+); 152 subjects were affected by EH without SM (EH SM-); and 40 subjects were normotensive (NT). Subjects with PA had the highest plasma resistin levels among the four groups (P < 0.01). Plasma resistin concentration was significantly higher in PA subjects when compared with EH SM+ individuals (P < 0.01) and EH SM- subjects (P < 0.01). PA subjects showed the higher LV mass and left atrium than EH individuals, irrespectively of the presence of SM (P < 0.01 for both). Plasma resistin levels was significantly correlated with ejection fraction and LV end-diastolic volume. The prevalence of SM was higher in PA subjects than in those with EH (25.4 vs. 20.3%). Our data suggest that elevated aldosterone levels is associated with elevated circulating resistin levels and cardiac morphological changes independently of the presence of SM.

Is retinal arteriolar–venular ratio associated with cardiac and extracardiac organ damage in essential hypertension?

Whether retinal microvascular disease is associated with markers of cardiac and extracardiac organ damage in human hypertension is still unclear. We examined the relationship between retinal arteriolar-venular ratio (AVR) and left ventricular hypertrophy, carotid atherosclerosis and microalbuminuria in essential hypertension. A total of 386 untreated and treated uncomplicated essential hypertensive individuals (mean age 56 +/- 13 years) consecutively attending our hospital outpatient hypertension clinic were considered for the analysis. All individuals underwent extensive clinical and laboratory investigations, including retinal AVR evaluation by a fully automated computer-assisted method, echocardiography and carotid ultrasonography. Mean retinal AVR was 0.790 +/- 0.079 (range 0.530-0.990). In univariate analyses, AVR showed a significant inverse association with left ventricular mass index (r = -0.15, P = 0.002) and carotid intima-media thickness (IMT) (r = -0.12, P = 0.02); no relationship with microalbuminuria was found. Overall, left ventricular mass index and carotid IMT as well as microalbuminuria, either as continuous or categorical variables, did not show significant differences across AVR quartiles. Moreover, a multivariate analysis failed to demonstrate independent correlations of carotid IMT and left ventricular mass index (P = 0.06 for both) with AVR. Finally, when patients were categorized according to the presence or absence of organ damage, with or without left ventricular hypertrophy (0.783 +/- 0.077 vs. 0.795 +/- 0.081), carotid plaques (0.789 +/- 0.079 vs. 0.791 +/- 0.079), carotid IMT (0.791 +/- 0.077 vs. 0.788 +/- 0.082) or microalbuminuria (0.791 +/- 0.080 vs. 0.777 +/- 0.073), no significant intergroup differences in AVR values were found. Our findings provide further evidence that retinal AVR is of limited value in identifying hypertensive patients at high cardiovascular risk related to cardiac and extracardiac organ damage.

The incremental effect of obstructive sleep apnea syndrome on right and left ventricular myocardial performance in newly diagnosed essential hypertensive subjects

Obstructive sleep apnea syndrome (OSAS) may predispose patients to congestive heart failure, suggesting a deleterious effect of OSAS on myocardial contractility. We investigated whether essential hypertensive individuals with OSAS are characterized by decreased right and left ventricular myocardial performance. Our study population consisted of 45 consecutive patients with newly diagnosed untreated stage I-II essential hypertension suffering from OSAS (35 men, aged 49+/-8 years) and 48 hypertensives without OSAS, matched for age, sex, level of blood pressure, heart rate, body mass index and smoking status. All subjects underwent polysomnography and echocardiography. Right and left ventricular functions were evaluated using the myocardial performance index (MPI). Right and left ventricular functions were altered in hypertensives with OSAS. The mean right MPI was 0.26+/-0.11 in hypertensives without OSAS and 0.51+/-0.16 in hypertensives with OSAS (P<0.01). The mean left MPI values were 0.29+/-0.07 and 0.44+/-0.13, respectively (P<0.01). Right and left MPI correlated positively and significantly with apnea-hypopnea index (rho=0.40, P=0.002).OSAS is associated with impaired right and left ventricular function. These phenomena were independent of hypertension.

Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension

The aim of the present study is to determine and correlate adiponectin, homocysteine, nitric oxide, and ADP-induced platelet aggregation levels in untreated patients with essential hypertension and healthy individuals. A total of 36 individuals, 23 untreated patients with essential hypertension and 13 healthy individuals, were included in the scope of this study. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum adiponectin and TNF-alpha levels. The levels of serum homocysteine were measured by using competitive chemiluminescent enzyme immunoassay. Serum concentrations of hsCRP were measured by the Nephelometer. Plasma nitrite, nitrate, and total nitric oxide (NOx) levels were determined by colorimetric method. Homocysteine and hsCRP levels in patients with essential hypertension were found to be significantly higher than those in the control group (P = 0.02, P = 0.001, respectively). The average platelet aggregation levels in patient group were higher than control group, but there were no statistically significant differences between them (P > 0.05). In addition, in patients with essential hypertension adiponectin and nitrite levels are significantly lower than control group (P < 0.001, P = 0.045, respectively). We have also found significant correlations between nitrite-platelet aggregation amplitude, nitrite-platelet aggregation slope, nitrite-adiponectin, homocysteine-platelet aggregation amplitude, and sistolic blood pressure-platelet aggregation amplitude levels (r = -0.844; P < 0.001, r = -0.680; P = 0.011, r = 0.454; P = 0.05, r = 0.414; P = 0.05, r = 0.442; P = 0.035, respectively). Increased homocysteine and decreased adiponectin serum levels in patients with essential hypertension correlate well with changes in ADP-induced conventional platelet aggregation. This association may potentially contribute to future thrombus formation and higher risks for cardiovascular events in hypertensive patients.

Effects of opioid blockade on nociceptive flexion reflex thresholds and nociceptive responding in hypertensive and normotensive individuals

Hypertension and risk for hypertension have been associated with reduced pain sensitivity. It has been hypothesised that endogenous opioids contribute to this hypertensive hypoalgesia. The nociceptive flexion reflex can be used as a tool to investigate modulation of nociceptive transmission at spinal level. The current study employed a double-blind placebo-controlled design to compare the effects of naltrexone, an opioid antagonist, and placebo on nociceptive flexion reflex thresholds and nociceptive responding in unmedicated patients with essential hypertension and normotensive individuals. Neither nociceptive flexion reflex thresholds nor nociceptive responding differed between hypertensives and normotensives during placebo or naltrexone. These data provide no support for the hypothesis that essential hypertension is characterised by higher levels of endogenous opioids in the central nervous system and reveal no association between blood pressure status and nociceptive flexion reflex responses.

Nondipping Blood Pressure Patterns among Individuals with Essential Hypertension: A Review of the Literature

Researchers have discovered that blood pressure (BP) varies in a diurnal manner throughout a 24-hour period, being higher during the day and lower at night. Most people have a dipping BP pattern characterized by a nighttime BP that is 10-20% lower than their daytime BP. Individuals who experience a less than 10% reduction in nighttime BP are described as having a nondipping BP pattern. Although controversial, there is a growing body of evidence suggesting that a nondipping BP pattern is associated with a greater risk of target organ damage among individuals with essential hypertension. To review the literature on the most common factors associated with nondipping BP patterns among individuals with essential hypertension. CINAHL (1982-March 2006), PubMed (1950-March 2006) and Cochrane Library (1966-March 2006) databases were searched using the keywords: dipper, dipping, nondipper, nondipping, ambulatory blood pressure monitoring, ABPM, hypertension, essential hypertension, high blood pressure, blood pressure, nocturnal blood pressure, nighttime blood pressure, diurnal blood pressure, and blood pressure patterns. Published studies, abstracts, dissertations as well as the reference lists of retrieved articles were reviewed. Studies were included if they involved subjects with only treated or untreated essential hypertension or those with samples of both nomotensive and treated or untreated essential hypertensive individuals. Additionally, studies needed to evaluate 24-hour, daytime and nighttime BP patterns. There is some evidence to suggest advanced age, African-American ethnicity, female sex, postmenopausal status, sodium sensitivity, sleep apnea, sleep quality, anger, hostility, depression, stress, social support, and socioeconomic status have an association with nondipping BP patterns. Knowledge of the potential factors associated with an altered nighttime BP pattern is of importance because it can help identify persons at risk for nondipping BP patterns and potential target organ damage. Furthermore, knowledge of these factors associated with a nondipping BP profile will lay the foundation for interventions to prevent/treat alterations in nighttime BP patterns.

The incremental effect of obstructive sleep apnoea syndrome on arterial stiffness in newly diagnosed essential hypertensive subjects

Although obstructive sleep apnoea syndrome (OSAS) is accompanied by an increased atherosclerotic cardiovascular disease burden, its relationship with arterial stiffness is not yet well determined. We investigated whether essential hypertensive individuals with OSAS are characterized by increased arterial stiffness. Our study population consisted of 46 consecutive patients with newly diagnosed untreated stage I-II essential hypertension suffering from OSAS (35 men, aged 49 +/- 8 years) and 53 hypertensive individuals without OSAS, matched for age, sex, and smoking status. All subjects underwent polysomnography, echocardiography and aortic stiffness evaluation by means of carotid-femoral pulse wave velocity (c-fPWV) measurements. Hypertensive subjects with OSAS [apnoea/hypopnoea index (AHI)>or =5] compared with hypertensive subjects without OSAS (AHI < 5) demonstrated increased levels of body mass index (31.4 +/- 4 versus 29.3 +/- 4 kg/m2, P = 0.015), office systolic/diastolic blood pressure (151/99 versus 145/94 mmHg, respectively, P < 0.05, for both cases) and relative wall thickness (RWT; 0.46 +/- 0.06 versus 0.42 +/- 0.07, P=0.010). Hypertensive subjects with OSAS compared with those without OSAS had significantly increased c-fPWV by 9% (8.56 +/- 0.49 versus 7.85 +/- 0.93 m/s, P=0.001) and this difference remained significant even after adjustment for confounders (P=0.04). In the total study population, c-fPWV was correlated with age (r=0.35, P=0.015), office systolic blood pressure (r=0.30, P=0.007), RWT (r=0.30, P=0.03), logAHI (r=0.389, P=0.0001) and minimum oxygen saturation (r=-0.418, P=0.0001). OSAS has a significant incremental effect on aortic stiffening in the setting of middle-aged essential hypertensive subjects. This finding suggests that the presence of OSAS in a hypertensive patient accelerates vascular damage, increasing cardiovascular risk.

Association of the β2-adrenergic receptor gene with essential hypertension in the non-Han Chinese Yi minority human population

The human beta2-adrenergic receptor (ADRB2) gene is a candidate for contributing to the pathophysiology of essential hypertension. The aims of the present study were to investigate the associations of differing single nucleotide polymorphisms (SNPs) and haplotypes of the ADRB2 gene promoter and coding regions with essential hypertension in genetically homogeneous Hani and Yi minority groups that are non-Han Chinese. Four SNPs in the regulatory and seven SNPs in the coding region were genotyped in 271 essential hypertension individuals and 267 controls, and eight haplotypes in the regulatory and five haplotypes in the coding region were determined and tested for association using the likelihood test statistic. There were significant associations of essential hypertension with separate SNPs located in both the regulatory and coding regions in the Yi minority group. In contrast, no associations of essential hypertension were detected with any of single SNPs in the Hani minority group. There is a significant difference in haplotype frequency distributions between the hypertensive participants and the controls in two groups (P < 10). The results indicate that variants at the ADRB2 locus may play a role in the pathophysiology of hypertension specifically in the Yi minority group.

Ambulatory blood pressure, asymptomatic cerebrovascular damage and cognitive function in essential hypertension

Prolonged exposure to elevated blood pressure (BP) can lead to both structural (white matter lesions (WML) or infarctions) and functional changes in the brain. We studied in previously diagnosed essential hypertensive individuals if diurnal BP variation and ambulatory BP (ABP) profile (daytime, night time and 24-h BP averages) were related to evidence of WML, the presence of 'silent' infarcts, and cognitive performance. A group of 86 patients (mean age 57.4+/-10 years, range 40-80) were first screened for hypertension-related organ damage and underwent 24-h ABP monitoring, magnetic resonance imaging (MRI) of the brain, and a comprehensive neurocognitive assessment. Age and ABP profile were related to more periventricular, but not subcortical, WML and to presence of lacunar infarctions on MRI. After correction for demographical group differences, no association was found between night time dipping of BP on the one hand and both WML load and cognitive parameters (verbal memory, sensorimotor speed, cognitive flexibility) on the other. The presence of lacunar infarctions, however, predicted lower performance on verbal memory. Furthermore, daytime and 24-h pulse pressure averages were associated with pWML, whereas systolic BP and mean arterial pressure (MAP) for daytime, night-time and 24-h periods were higher in patients with lacunar infarctions. Notwithstanding the large variability of WML in this sample, the evidence of a connection between diurnal BP variation and early target organ damage in the brain was not convincing. However, the ABP profile may be predictive of cerebral lesion type.

Ambulatory blood pressure, target organ damage and left atrial size in never-treated essential hypertensive individuals

To investigate the relationship between ambulatory blood pressure and different markers of target organ damage with left atrial size in never-treated essential hypertensive individuals. A total of 519 grade 1 and 2 hypertensive patients (mean age 46 +/- 12 years), referred for the first time to our outpatient clinic, underwent routine examinations: 24-h urine collection for microalbuminuria, ambulatory blood pressure monitoring over two 24-h periods in 4 weeks, echocardiography and carotid ultrasonography. Left atrial diameter was increased in 17.3% of patients. No significant differences were found between subjects with and without increased left atrial size with regard to sex, duration of hypertension, clinic and mean 48-h ambulatory blood pressure, and daytime and night-time values. Compared with 429 patients with normal left atrial size, the 90 patients with enlarged left atria were older, had higher body mass index, were more frequently smokers, and included more individuals with the metabolic syndrome. The prevalence of left ventricular hypertrophy, of intima-media thickening, but not of microalbuminuria was significantly higher in subjects with increased left atrial size. Left atrial enlargement is not an early echocardiographic finding in relatively young never-treated hypertensive individuals, as its prevalence is lower than that of well-validated markers of target organ damage, and it is unrelated to ambulatory blood pressure. Overweight, left ventricular hypertrophy, carotid intima-media thickening and metabolic syndrome are independent predictors of left atrial dimension, suggesting that changes in left atrial size represent an adaptive response when high blood pressure is associated with other cardiovascular or metabolic abnormalities.

Genetic variations in six candidate genes for insulin resistance in Korean essential hypertensives

Hypertension is a complex disease with strong genetic influences. Essential hypertension has been shown to be associated with insulin resistance. To clarify the genetic basis of insulin resistance in hypertension, case‐control association studies were performed to examine candidate genes for insulin resistance in hypertension. Polymorphisms investigated were the BstO I polymorphism of the (β3‐adrenergic receptor (ADRB3) gene, the Xba I polymorphism of the glycogen synthase (GS Y) gene, the Dde I polymorphism of the protein phosphatase 1 G subuit (PP1G) gene, the BstE II polymorphism of the glucagon receptor (GCG‐R) gene, the Pst I polymorphism of the insulin (INS) gene and the Acc I polymorphism of the glucokinase (GCK) gene. No significant differences were observed in the distribution of alleles and genotypes of the ADRB3, GS Y, PP1G, GCG‐R, INS, and GCK genes between hypertensive and normotensive groups. Although the frequencies in each of these polymorphisms were not significantly different between essential hypertensive and normotensive individuals, our results may provide additional information for linkage analysis and associative studies of disorders in carbohydrate metabolism or in cardiovascular disease.

Dissociation between microalbuminuria and common carotid thickness in essential hypertensive men.

The reasons why microalbuminuria (albuminuria > or = 15 microg/min), an expression of a renal microcirculatory abnormality, predicts cardiovascular disease in essential hypertension are unsettled. To test the hypothesis that microalbuminuria represents a marker of subclinical atherosclerosis, we evaluated its association with common carotid artery (CCA) intima media thickness (IMT), a measure of preclinical atherosclerosis and an independent predictor of cardiac and cerebrovascular events, in uncomplicated essential hypertensive individuals. Albuminuria, ultrasonographic CCA IMT (the mean of six bilateral far wall measurements within 1.5 cm proximally to the flow divider), brachial blood pressure (BP), smoking habits and lipids were evaluated in 136 stage 1-3 untreated essential hypertensive men free of cardiovascular disease. CCA IMT did not differ between normo- (n = 99) and microalbuminuric (n = 37) patients. The correlation between CCA IMT and albuminuria was not significant, and the prevalence of microalbuminuria across IMT quartiles was not different. Microalbuminuric patients showed higher systolic BP and that parameter was the only independent correlate in a multivariate logistic regression model including also age, CCA IMT, diastolic BP, lipids and smoking habits as independent variables and microalbuminuria as the dependent one. This cross-sectional study in hypertensive subjects free of cardiovascular disease has shown a dissociation between microalbuminuria and CCA IMT, a surrogate measure of subclinical atherosclerosis, and a parameter linearly related to cardiovascular events. The data do not support the theory of microalbuminuria as a surrogate measure of subclinical atherosclerosis, while confirming the importance of systolic BP levels as an independent correlate of increased albuminuria in essential hypertension. Journal of Human Hypertension (2000) 14, 831-835

Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells and increases soluble ICAM-1 release in vivo.

We evaluated whether angiotensin II (Ang II) influenced intercellular adhesion molecule (ICAM)-1 expression by human vascular endothelial cells derived from umbilical cord veins (HUVECs) and plasma soluble ICAM-1 levels in vivo. Cultured HUVECs were incubated with Ang II (from 10(-9) to 10(-6) mol/L) with or without candesartan and PD12319 (inhibitors of Ang II AT(1) and AT(2) receptors, respectively) for various times up to 4 hours. Total RNA was then extracted from HUVECs, and Northern blots were probed with a 1.9-kb ICAM-1 cDNA fragment. HUVEC supernatants were used to assess soluble ICAM-1 release by ELISA. Northern blot analysis detected a strong increase of ICAM-1 mRNA after 2-hour incubation with Ang II. The response was inhibited by candesartan. Soluble ICAM-1 release by HUVECs also increased (P<0. 002) after 2-hour Ang II stimulation. In vivo, Ang II (at an initial rate of 1.0 ng. kg(-1). min(-1), to be increased each 30 minutes by 2.0 ng. kg(-1). min(-1) to the final rate of 7.0 ng. kg(-1). min(-1)) was infused in 8 normotensive and 12 essential hypertensive individuals. In the latter, Ang II was reinfused after 4 weeks on either placebo (n=3), losartan (50 mg UID, n=5), or atenolol (50 mg UID, n=4) treatment. Plasma soluble ICAM-1 levels increased after Ang II infusion in hypertensives and normotensives (P<0.0001 after 90 minutes). Losartan reduced baseline soluble ICAM-1 levels (P<0.05) and Ang II-related ICAM-1 increments. Ang II upregulates ICAM-1 expression by HUVECs and stimulates in vitro and in vivo soluble ICAM-1 release. AT(1) receptor blockade inhibits such endothelial effects of Ang II.