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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abdominal obesity is a risk factor for cardiovascular disease worldwide, and it is becoming a dramatic issue for national health systems. Overweight and obesity are highly associated with multiple comorbidities, elevated blood pressure values, dyslipidaemia, reduced insulin sensitivity and alterations of large and minor vessels. Activation of the renin-angiotensin system (RAS) in adipose tissue may represent an important link between obesity and hypertension. Angiotensin II has been shown to play a role in adipocyte growth and differentiation. Adipocytes also secrete adiponectin, enhancing insulin sensitivity and preventing atherosclerosis. Blockade of the RAS with either an angiotensin-converting enzyme inhibitor or an angiotensin II receptor blocker results in a substantial increase in adiponectin levels and improved insulin sensitivity. Obesity-related hypertension needs a comprehensive approach to treatment including both weight loss and pharmacological therapies. Antihypertensive drugs prescription should be based on guidelines recommendations for management of hypertension, taking into account the growing evidences about the relationship between some antihypertensive drugs and the development of new-onset diabetes. This review discusses the role of RAS in the relationship between obesity, essential hypertension and insulin resistance.
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PMID:Obesity, essential hypertension and renin-angiotensin system. 1790 24

A dihydropyridine calcium (Ca) antagonist, azelnidipine (CAS 123524-52-7, Calblock), exhibits hypotensive effects for a prolonged duration, and has been reported to have a strong antiarteriosclerotic action due to its high affinity for vascular tissues and antioxidative action. It has also been reported that azelnidipine does not cause tachycardia associated with the baroreceptor reflex due to vasodilatation. In this study, the antiarteriosclerotic and cardiac hypertrophy-inhibitory effects, and the autonomic nervous activity in essential hypertension of azelnidipine were investigated. The study was performed using the following 2 protocols: 1) Pulse wave velocity (PWV), carotid arterial intima media thickness (IMT), echocardiography, high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), adiponectin, brain natriuretic peptide (BNP), and 8-isoprostane were measured after an initial treatment with azelnidipine. 2) The treatment was switched to azelnidipine in patients who had previously been under treatment with amlodipine for essential hypertension, and 123I-metaiodobenzylguanidine myocardial scintigraphy (123I-MIBG), measurements of plasma norepinephrine, atrial natriuretic peptide (ANP), and BNP, Holter electrocardiography, and heart rate variability analysis were performed. PWV, IMT, hs-CRP, IL-6, and TNF-alpha significantly decreased. The levels of 8-isoprostane, an antioxidative marker, were also significantly decreased, while adioponectin levels were significantly increased after the initial treatment with azelnidipine. After switching from amlodipine, azelnidipine exhibited a hypotensive effects comparable to amlodipine, and significantly decreased heart rate and the total number of extrasystoles. Noradrenaline levels and the LF/HF ratio were significantly decreased, and the washout rate was significantly reduced on 123I-MIBG myocardial scintigraphy. These findings suggest that azelnidipine inhibits the enhancement of sympathetic nervous activity and the progression of arteriosclerosis through its antioxidative effects.
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PMID:Clinical study with azelnidipine in patients with essential hypertension. Antiarteriosclerotic and cardiac hypertrophy-inhibitory effects and influence on autonomic nervous activity. 1819 91

We examined whether moxonidine influences lipid profile, insulin resistance, adiponectin levels, renal function and microalbuminuria in women with essential hypertension in a study of 55 non-diabetic hypertensive patients and 53 normotensive women. Hypertensive patients received moxonidine for 12 weeks. At baseline the hypertensive group had significantly higher mean blood pressure, low-density lipoprotein cholesterol, triglycerides, total cholesterol, fasting glucose, urinary albumin excretion and homeostasis model assessment of insulin resistance (HOMA-IR), together with significantly lower mean high-density lipoprotein cholesterol, creatinine clearance and serum adiponectin than the normotensive group. Moxonidine significantly decreased blood pressure, fasting glucose, triglycerides, total cholesterol, HOMA-IR and albumin excretion, but significantly increased serum adiponectin. The change in adiponectin level was negatively correlated with the change in HOMA-IR. Moxonidine treatment may improve unfavourable metabolic status related to insulin resistance by increasing adiponectin levels in patients with essential hypertension. Since it can improve adiponectin levels, it may be used in the antihypertensive treatment of patients at high risk of diabetes and cardiovascular disease.
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PMID:Effects of sympatholytic therapy with moxonidine on serum adiponectin levels in hypertensive women. 1823 Feb 71

Obesity is the main intermediate phenotype of primary hypertension (PH), and increased fat mass is directly related to target organ damage (TOD) and metabolic syndrome (MS). The aim of the study was to assess the sensitivity and specificity of body mass index (BMI), percentile-based, definitions of obesity [BMI > 95th percentile (pc)], and overweight (BMI > 85th pc), and BMI thresholds for cardiovascular (cv) complications (BMIcv) described by Katzmarzyk et al. (Pediatrics 114:198-205, 2004) in predicting risk of TOD and MS in 122 adolescents with PH. Our results indicated that the prevalence of left ventricular hypertrophy (LVH) and carotid intima-media thickness (cIMT) above 2 standard deviations (SDS) was the same, irrespective of the criteria used. BMIcv was more sensitive as a marker of LVH than were the cut-off values of the 85th pc and 95th pc of BMI (87.5%, 75%, 62.5%, respectively; P < 0.0001). BMIcv thresholds and cut-off values of the 85th pc of BMI were of the same sensitivity in predicting the presence of MS (95.8% and 95.8%, respectively) and were more sensitive than the cut-off values of the BMI 95th pc (87.5%; P = 0.02). Metabolic abnormalities, including insulin resistance, were more marked in patients with greater BMI, irrespective of cut-off value. However, only when a stratification system using the 85th pc of BMI was used, were the differences significant for a homoeostasis model assessment for insulin resistance (HOMA-IR) and for serum concentrations of high-density lipoprotein (HDL)-cholesterol, triglycerides and adiponectin. We concluded that BMIcv is more sensitive for diagnosing the presence of LVH and that the cut-off value of the 85th pc of BMI is more sensitive for predicting presence of MS in children with PH.
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PMID:Different BMI cardiovascular risk thresholds as markers of organ damage and metabolic syndrome in primary hypertension. 1825 58

Studies performed during the last decade indicate that adipose tissue is not only a site of triglyceride storage but also an active endocrine organ which secretes many biologically active mediators referred to as "adipokines". In contrast to many adipokines which are overproduced in obese individuals and exert deleterious effects on insulin sensitivity, lipoprotein metabolism and cardiovascular system, such as leptin, tumor necrosis factor-alpha, plasminogen activator inhibitor-1, resistin, etc., adiponectin seems to be a unique adipokine which is produced in lower amounts in obese than in lean subjects and possesses predominantly beneficial activities, i.e. increases insulin sensitivity, stimulates fatty acid oxidation, inhibits inflammatory reaction and induces endothelium-dependent nitric oxide-mediated vasorelaxation. Adiponectin binds two receptors, AdipoR1 and AdipoR2. Adiponectin knockout mice exhibit various manifestations of the metabolic syndrome such as insulin resistance, glucose intolerance, hyperlipidemia, impaired endothelium-dependent vasorelaxation and hypertension, as well as augmented neointima formation after vascular injury. Clinical studies indicate that plasma adiponectin concentration is lower in patients with essential hypertension and ischemic heart disease. Raising endogenous adiponectin level or increasing the sensitivity to this hormone may be a promising therapeutic strategy for patients with metabolic and cardiovascular diseases. Among currently used drugs, thiazolidinediones (peroxisome proliferator activated receptor gamma agonists) are most effective in elevating adiponectin level.
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PMID:Adiponectin and its role in cardiovascular diseases. 1833 52

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.
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PMID:Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension. 1900 85

Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) gamma. Stimulation of PPAR gamma has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9+/-5.6 to 58.1+/-5.4 pg/mL) and perindopril (74.1+/-4.7 to 64.7+/-5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9+/-4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR gamma stimulating activity is equivalent to ACE-I for the treatment of hypertension.
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PMID:Effects of ARB or ACE-inhibitor administration on plasma levels of aldosterone and adiponectin in hypertension. 1960 54

Accumulating clinical evidence indicates that impaired glucose tolerance is a common phenomenon in essential hypertension. Although recent evidence underscores the role of heme-oxygenase (HO) in diabetes, its effects on insulin sensitivity and glucose metabolism in spontaneously hypertensive rat (SHR), a model of essential hypertension with characteristics of metabolic syndrome including insulin resistance/impaired glucose metabolism remains largely unclear. Here we report the effects of the HO inducer, hemin, and the HO blocker, chromium-mesoporphyrin on insulin sensitivity and glucose metabolism in SHRs. Adult SHRs were severely hypertensive but normoglycemic. Hemin therapy lowered blood pressure, increased plasma insulin, decreased glycemia, and enhanced insulin sensitivity by improving glucose tolerance (ip glucose tolerance test) and insulin tolerance (ip insulin tolerance test) but reduced insulin resistance (homeostasis model assessment index). These effects were accompanied by increased gastrocnemius muscle HO-1, HO activity, cGMP, cAMP alongside antioxidants including bilirubin, ferritin, superoxide dismutase, catalase, and the total antioxidant capacity, whereas oxidative/inflammatory mediators like 8-isoprostane, nuclear-factor-kappaB, activating-protein-1, activating-protein-2, c-Jun-NH2-terminal-kinase, and heme were abated. Furthermore, hemin reduced proteinuria/albuminuria and enhanced the depressed levels of adiponectin, AMP-activated protein-kinase, and glucose transporter-4 in SHRs, suggesting that although SHRs are normoglycemic, insulin signaling and renal function may be impaired. Contrarily, the HO inhibitor chromium-mesoporphyrin exacerbated oxidative stress, aggravated insulin resistance, glucose tolerance, insulin tolerance and nephropathy. Hemin also enhanced HO signaling in Wistar Kyoto and Sprague Dawley rats and increased insulin sensitivity albeit less intensely than in SHRs, suggesting greater selectivity of HO in SHRs with dysfunctional insulin signaling. These results suggest that perturbations of insulin signaling may be a forerunner to hyperglycemia in essential hypertension. By concomitantly potentiating insulin-sensitizing agents, suppressing insulin/glucose intolerance, and abating oxidative stress, HO inducers may prevent metabolic and cardiovascular complications in essential hypertension.
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PMID:Up-regulating the heme oxygenase system with hemin improves insulin sensitivity and glucose metabolism in adult spontaneously hypertensive rats. 2001 31

Low-grade inflammation plays a role in the pathogenesis of primary hypertension (PH) and target organ damage (TOD). We evaluated the profile of inflammatory mediators (CRP, RANTES, MIP-1beta, MIP-1alpha, MCP-1, IL-6, angiogenin, adiponectin) in 30 healthy children (12.7 +/- 3.3 years) and 44 patients with untreated PH (13.7 +/- 2.7 years; n.s). Patients had greater concentrations of CRP, MIP-1beta, and RANTES than controls (all p < 0.05). Children with metabolic syndrome (MS) had greater CRP than children without MS (p = 0.007) and CRP correlated with number of MS criteria, body mass index (BMI), visceral fat, deep subcutaneous fat assessed by magnetic resonance imaging, carotid intima-media thickness (cIMT), left ventricular mass index, and markers of oxidative stress. RANTES correlated with cholesterol, LDL cholesterol, ApoB, and ApoB/ApoA1. Angiogenin correlated with BMI, waist circumference, visceral fat, uric acid, and patients with cIMT>2SD had greater concentration of angiogenin than those with normal cIMT (p = 0.03). Adiponectin was lower in patients with cIMT>2SD than in those with normal cIMT (p = 0.02). No model explaining variability of TOD has been built. Elevated RANTES and MIP-1beta and normal IL-6 and TNF-alpha levels indicate a vascular inflammatory process. Lack of correlation between CRP and chemokines suggests that vascular inflammation in PH precedes the systemic inflammatory changes.
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PMID:Inflammatory activation in children with primary hypertension. 2049 30

Coexistence of hypertension and diabetes mellitus (DM) increases the risk of cardiovascular disease. However, factors associated with future development of DM have not been well elucidated in patients already having essential hypertension. This study prospectively included 168 patients (mean age 41 +/- 7 years, 112 men) with essential hypertension. All patients did not have DM and vascular or renal complications initially. Baseline demographic data, blood pressure, body mass index, and antihypertensive agents were carefully evaluated and serum high-sensitivity C-reactive protein (hsCRP) was measured at the beginning of the study. All of the patients were followed for at least 6 months. The study endpoint was occurrence of new DM. After a mean follow-up period of 32 +/- 10 months, 22 subjects (13.1%) developed new DM. Patients with new DM had higher baseline glucose (105.2 +/- 11.8 vs 94.2 +/- 8.0 mg/dl, P < 0.001), triglyceride level (213.7 +/- 112.4 vs 155.6 +/- 83.2 mg/dl, P = 0.04), log hsCRP (0.31 +/- 0.44 vs 0.19 +/- 0.25 mg/dl, P = 0.016), and lower high-density lipoprotein (40.2 +/- 7.8 vs 46.6 +/- 14.4 mg/dl, P = 0.045). Total cholesterol, low-density lipoprotein, homeostasis model assessment index, and adiponectin were not different in patients with or without new DM. Among antihypertensive agents, only use of beta-blocker was significantly associated with new DM (P = 0.008). Multivariate Cox regression analysis showed log hsCRP (hazard ratio [HR] 9.77, 95% confidence interval [CI] 2.97-32.10, P < 0.001), age (HR 1.21, 95% CI 1.06-1.38, P = 0.004), and baseline glucose level (HR 1.11, 95% CI 1.06-1.15, P < 0.001) to be independent predictors for occurrence of new DM. High-sensitivity CRP was an independent factor for future development of DM in essential hypertensive patients. Increased inflammation might have a key role in the pathogenesis of DM in hypertension.
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PMID:Increased C-reactive protein is associated with future development of diabetes mellitus in essential hypertensive patients. 2067 60


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