UMLS:C0085580 - FACTA Search

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

The effects of nebivolol, a new beta-blocker with vasodilating properties, and hydrochlorothiazide (HCTZ) as monotherapies and in combination on BP and plasma lipids, lipoproteins and apolipoproteins were compared with placebo in a parallel 3 x 4 factorial design study. After an eight week wash-out period, 240 patients with primary hypertension were randomised to receive either placebo, nebivolol 1, 5 or 10 mg, HCTZ 12.5 or 25 mg or one of the six possible combinations of nebivolol and HCTZ. Twenty patients were assigned to each of the 12 parallel groups. After 12 weeks of treatment, there was a significant dose-related reduction in BP among all active treatment groups. Apart from a slight and isolated increase in triglycerides with HCTZ 12.5 mg, lipid, lipoprotein and apolipoprotein levels as well as lipoprotein and apolipoprotein ratios were not significantly modified by 12 week active treatments when compared with placebo treatment. The results of this multifactorial study with 12 small sample size groups, suggest that nebivolol as monotherapy and in combination with HCTZ does not cause deleterious effects on the lipid profile.
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PMID:Placebo-controlled comparison of the effects of nebivolol and low-dose hydrochlorothiazide as monotherapies and in combination on blood pressure and lipid profile in hypertensive patients. 802 9

The aim of the study was to investigate the effect of a new selective alpha 1-adrenoreceptor blocker doxazosin on blood pressure, serum lipids and lipoproteins in patients with essential hypertension. The study was done in 32 out-patients with mild-to-moderate hypertension (22 men and 10 women, mean age 45.6 +/- 10.1). After 2-week placebo period the patients were given doxazosin in increasing doses from 1 to 8 mg daily for 6 to 14 weeks (mean daily dose 2.24 +/- 1.6 mg). Twenty-nine patients completed the study. The active treatment caused highly significant drop in systolic and diastolic blood pressure both in supine and standing positions. No orthostatic hypertension was noted. There was also a statistically significant decrease in serum total cholesterol, VLDL-cholesterol, and triglyceride levels and increase in the positive prognostic lipid indicators. HDL3-cholesterol and apolipoprotein AI levels as well as HDL/total cholesterol ratio. Accordingly, the statistically significant decrease of the so called atherogenic index was noted. The drug was well tolerated and only one patient dropped from the study because of side effects. The authors conclude that doxazosin appears to be an effective and well tolerated antihypertensive drug with a favorable effect on lipid metabolism. It may be particularly useful in hypertensive patients with coexisting lipid abnormalities.
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PMID:[Doxazosin (alpha 1-adrenoreceptor antagonist) used in primary hypertension and it's beneficial effect on lipid metabolism]. 823 Sep 80

Apolipoprotein is now a new biochemical marker for evolution of atherosclerosis, even better than lipid fraction. We studied seric apolipoprotein A and B (Apo A, B) on 50 cases with complicated obesity, with ages between 37-52 years, and 15 males and 35 females. Selection criteria were: android constitution, obesity, essential hypertension (EHT). We also made statistical correlations on IBM PC compatible computer using chi-square test. We correlated glycoregulation abnormalities with body mass index (BMI > 25) with meaningfully value (p < 0.005) or with complicated EHT less meaningfully (p < 0.2). On this background, we appreciated the predictive value of seric levels of Apo A, B and Apo B/A ratio > 1. EHT correlates with low levels of seric Apo A very meaningfully (p < 0.0001) and this association is higher correlated when added ICD (P < 0.00001). There is no significant relationship between high levels of seric Apo B and EHT in our study, but it is significant for Apo B/A > 1 (p < 0.0001). EHT with seric cholesterol are not correlated (p:NS). Our conclusion is that seric Apo A and Apo B/A are statistical predictive risk factors for complicated EHT on android obese persons (X syndrome).
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PMID:[Apolipoproteins-a cardiovascular risk factor within the context of syndrome X]. 945 12

Recent developments in molecular biological techniques allowed us to examine the genetic risk factors responsible for essential hypertension. The candidate gene approach revealed that several gene polymorphisms increase the relative risk for hypertension. Most genetic studies, however, examined only young subjects but not elderly ones. To examine the importance of gene polymorphisms in elderly hypertension, we carried out a case-control study and compared the odds ratio for hypertension between young (< 60) and elderly (> or = 60) subjects. The participants of this study were recruited from the outpatients of Osaka University Medical School with informed consent. We examined the following polymorphisms as candidates: the angiotensinogen (AGT/M235T), angiotensin converting enzyme (ACE I/D), angiotensin II type 1 (AT1/A1166C) and type 2 (AT2/C3123A) receptors, alpha-adducin (adducin/Gly460Trp), methylenetetrahydrofolate reductase (MTHHR/C677T), and apolipoprotein (apoE/epsilon 4, apoE/T-491A). In young subjects, the AGT/T235 allele significantly increased the odds ratio for hypertension but not in elderly subjects. In young males, the AT2/A3123 allele was also associated with hypertension but not in females or in elderly subjects. Other associations between polymorphism and hypertension did not reach a significant level. To sum up, it was revealed that some polymorphisms increase the susceptibility for hypertension but others do not, which suggests that there is heterogeneity in the genetic involvement of polymorphism due to aging.
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PMID:[Genetic analysis of candidate gene polymorphisms in elderly hypertension]. 1055 62

As renin is the key enzyme of the renin-angiotensin-aldosterone system, the renin gene (REN) represents a good candidate quantitative trait locus for investigations aimed at uncovering the molecular and genetic influences implicated in the molecular etiology of essential hypertension. Among the various polymorphic markers that are available at the REN gene locus, an MboI dimorphic site located in the ninth intron of the REN gene has previously been shown to be significantly associated with a family history of hypertension in a Japanese population and with direct clinical diagnosis of essential hypertension in a Gulf population. We determined MboI allele and genotype distributions in a sample population of 349 (178 men, 171 women) hyperlipidaemic US Caucasians (mean age 55.4+/-13.1 yr), comprising 122 hypertensive and 227 normotensive subjects. A statistically significant association was found between alleles on which the MboI site was present [MboI(+)] and clinical diagnosis of hypertension. REN MboI(+) alleles are thus in linkage disequilibrium with genetic influences that contribute to increased individual susceptibility to hypertension of hyperlipidaemic patients (with an associated odds ratio of 2.15, 95% CI: 1.34-3.45). This positive association does not seem to occur through the effect of classical risks factors represented by lipid, lipoprotein and apolipoprotein levels.
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PMID:Renin gene MboI dimorphism is a discriminator for hypertension in hyperlipidaemic subjects. 1058 Mar 95

The human renin gene (REN) is a good candidate in studies aimed at unravelling the genetic basis of essential hypertension and stroke. We previously established that both a BglI and an MboI dimorphisms (located respectively in the first and ninth introns of the REN gene) were associated with essential hypertension in a population of hyperlipidaemic US subjects. In this association (retrospective case-control) study, we investigated the haplotype distribution of alleles defined by the combination of REN BglI and MboI dimorphic sites in 329 hyperlipidaemic US Caucasian subjects referred to UCSF Medical Center (140 hypertensives, 141 normotensives, and 48 hypertensive patients who had suffered a stroke). A statistically significant association was found between alleles determined by both (BglI(-)/MboI(+)) and (BglI(+)/MboI(+)) haplotypes and clinical diagnosis of EHT (combined odds ratios, OR = 3.35, corrected P < 10(-7)). Haplotypes (-,+) and (+,+) were also found to be associated with clinical diagnosis of stroke (OR = 4.31, P < 10(-7)). These associations do not occur through the effects of classical risk factors related to lipid, lipoprotein and apolipoprotein levels. We conclude that variations of the REN (or of a nearby) gene that may be in linkage disequilibrium with REN (BglI(-)/MboI(+)) and (BglI(+)/MboI(+)) alleles could play a role in contributing to increased individual's genetic susceptibility to EHT and to stroke. Journal of Human Hypertension(2001) 15, 49-55
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PMID:Haplotypes of the human renin gene associated with essential hypertension and stroke. 1122 2

The aim of the study is to investigate serum lipoproteins abnormalities including low-density lipoprotein (LDL) particle size, and their relationship with other cardiovascular risk factors in men with essential hypertension. Plasma glucose and serum insulin levels during oral glucose tolerance test (OGTT), serum lipoprotein(a), apolipoprotein (apo) A-I. apo B. cholesterol and triglycerides in serum and in lipoproteins, and LDL particle diameter were measured in thirty-eight consecutive newly-diagnosed non-diabetic untreated hypertensive men and 38 healthy male controls. Plasma glucose at baseline, 60 and 120 min during OGTT was significantly higher in patients than controls whereas serum insulin levels did not differ between patients and controls. Serum apo B and triglycerides were significantly raised in patients compared with controls (1.08 +/- 0.17 g/L [mean +/- SD] vs 0.97 +/- 0.22 g/L. p < 0.05, and 1.56 +/- 0.90 mmol/L vs 1.15 +/- 0.57 mmol/L, p < 0.05, respectively). Very-low-density lipoprotein (VLDL) triglycerides and LDL-cholesterol were increased in patients compared with controls (0.89 +/- 0.79 mmol/L and 0.54 +/- 0.35 mmol/L, p < 0.05, and 4.08 +/- 0.85 mmol/L and 3.60 +/- 0.92 mmol/L, p < 0.05, respectively) whereas high-density lipoprotein (HDL) cholesterol was lower in patients compared with controls 0.95 +/- 0.22 mmol/L and 1.07 +/- 0.20 mmol/L, p < 0.05). Adjustment for body mass index, abdominal/hip perimeter ratio and area under the glucose curve did not attenuate the relationship between hypertension and VLDL-triglycerides. Six patients and two controls had a mean LDL diameter < or = 25.5 nm and in the former serum triglycerides ranged from 1.86 mmol/L to 2.37 mmol/L. Mean LDL particle diameter in both patients and controls showed an inverse relationship with log-transformed serum triglycerides (r = - 0.51, p < 0.001 and r = - 0.47, p < 0.005, respectively). Among patients, those with serum triglycerides > or = [corrected] 1.58 mmol/L had a lesser mean LDL diameter than those with triglycerides above this threshold (25.78 +/- 0.47 nm vs 26.30 +/- 0.35 nm, p < 0.001). Higher plasma glucose, serum apo B and LDL-cholesterol as well as the decrease in serum HDL-cholesterol in patients with hypertension are consistent with high coronary heart disease risk. Not only mild hypertriglyceridemia but also high-normal serum triglycerides in themselves or as a surrogate of a predominance of small dense LDL particles in plasma convey an additional risk for cardiovascular disease in hypertensive patients even though routine plasma lipids are within or near normal range.
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PMID:Low-density lipoprotein particle size, triglyceride-rich lipoproteins, and glucose tolerance in non-diabetic men with essential hypertension. 1147 31

Etiopathogenesis of arterial hypertension and coronary disease involves interaction of numerous exogenous factors which determine the clinical course and therapeutic response in genetically predisposed individuals. The role of numerous cardiovascular risk factors has been reevaluated during the past few years, yet some unresolved issues and gaps still remain. One of the still insufficiently studied factors is lipoprotein (a) [Lp (a)] which belongs to a subclass of LDL lipoproteins. Its important component is apolipoprotein (a) which is structurally similar to plasminogen. This characteristic can be followed through evolution and is probably crucial for its physiologic but also pathophysiologic role. Actually, through its competition with plasminogen, Lp (a) interferes with the process of fibrinolysis and may contribute to tissue healing and restoration but also support and accelerate atherothrombotic process. Lp (a) concentration is stable and genetically determined in an individual and the indication that persons with elevated levels are permanently exposed to increased risk is supported by the data on twofold incidence of myocardial infarction in mothers of children with highest Lp (a) concentrations. Apart from competing with plasminogen via apolipoprotein (a), Lp (a) increases the activity of inhibitors of plasminogen-I activator and reduces the activity of transforming growth factor-beta. This results both in the absence of fibrinolysis and promotion of migration and proliferation of media smooth muscle cells, which are important in the onset of atherosclerotic process. Lp (a) binds to elastin via apolipoprotein B, resulting in oxidation and facilitated entry into macrophages and their transition into the so-called foam cells, also an important sign of early atherosclerosis. Although many pathophysiologic processes by which Lp (a) contributes to atherosclerosis have also been confirmed by animal experiments as well as by the presence of histologic evidence, clinical significance of elevated Lp (a) concentration is still questionable. However, results of prospective studies and metaanalyses were published few months ago and identified decisively Lp (a) as a factor that increases cardiovascular risk primarily in patients in whom other risk factors were also present. According to currently prevailing attitude, routine determination of Lp (a) is not justified and, according to most authors, its determination is useful in patients who had a cardiovascular incident at the age under 55 years, in those with recurrent coronary stenosis, or those with positive family history of such incidents. As Lp (a) is genetically determined, its detection in the early stages of essential hypertension might be a useful prognostic marker but a period of observation is still necessary for correct selection of hypertensive patients. Apart from the observation that hormone replacement therapy significantly decreases the Lp (a) level, there is currently no information on the effectiveness of either dietary or drug therapy. Due to Lp (a) antifibrotic effects, small aspirin doses may be beneficial to these patients, as well as B complex vitamins since hyperhomocysteinemia enhances atherogenicity of Lp (a). Therapeutic approach to patient with increased Lp (a) levels is currently based on as strict regulation of arterial pressure, glycemia and other dislipidemias as possible. In the present clinical practice, the elevated level of this lipoprotein indicates a patients with elevated cardiovascular risk, regardless of the fact whether Lp (a) is only a marker or an active factor of pathophysiologic process. Increased Lp (a) concentration may refer to the need for therapy, frequent monitoring and determination of even stricter aims for these individuals by selecting metabolically neutral and best tolerated drugs.
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PMID:[Lipoprotein (a)--a mysterious factor in atherogenesis]. 1267 78

The objective of this cross-sectional controlled study was to evaluate the intima-media thickness (IMT) of the common carotid artery (cIMT) and superficial femoral artery (fIMT), as well as the elastic properties of the common carotid artery, in children with essential arterial hypertension. The study included 49 children with newly detected essential hypertension [mean age 14.5 (range 6-20) years] and 61 healthy normotensive children [mean age 13.5 (range 6-20) years]. The cIMT and fIMT were evaluated by ultrasonography. The elastic properties of the carotid artery were calculated from actual blood pressure values, arterial dimensions, and carotid wall thickness. Hypertensive children had greater values of both cIMT (0.45+/-0.05 mm) ( P=0.0001) and fIMT (0.37+/-0.05 mm) ( P=0.005) than controls (0.41+/-0.04 and 0.33+/-0.06 mm, respectively). The internal systolic and diastolic diameters of the common carotid artery were also significantly greater in hypertensive patients. The distensibility and elasticity of the common carotid artery were significantly decreased in hypertensive patients, while arterial compliance was significantly greater than in controls. cIMT and fIMT correlated with systolic and pulse pressure values, body mass index (BMI), homocysteine, low high-density lipoprotein, and apolipoprotein AI. After subdividing the control group and patients according to BMI below or above the 95th percentile for age and sex, there were differences only between normal-weight normotensive children and the two groups of hypertensive children. The stepwise regression analysis showed that the predictive factor for cIMT was pulse pressure and for fIMT body mass and homocysteine. Hence, in newly diagnosed children with essential hypertension, functional and anatomical changes in elastic and muscular arteries are observed. Pulse pressure and biochemical risk factors for cardiovascular damage were predictors of vessel wall injury, even if it remained within the normal range. BMI is an important factor influencing IMT values.
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PMID:Intima-media thickness and arterial elasticity in hypertensive children: controlled study. 1513 71

The effect of barnidipine, a calcium channel blocker, on metabolic parameters is not well known. The authors conducted the present pilot study to evaluate the possible effects of barnidipine on parameters involved in atherogenesis, oxidative stress, and clotting activity. This open-label intervention study included 40 adult patients with essential hypertension who received barnidipine 10 mg once daily. Barnidipine significantly reduced systolic and diastolic blood pressure as well as isoprostane levels, which represent a reliable marker of oxidative stress. In contrast, barnidipine had a neutral effect on lipid profile and apolipoprotein levels, did not influence glucose homeostasis, had no effect on renal function, and did not cause any changes in electrolyte levels. Moreover, barnidipine did not affect either the clotting/fibrinolytic status (evaluated by measurement of fibrinogen, total plasminogen activator inhibitor, tissue plasminogen activator, and a2 antiplasmin) or the enzymatic activity of the inflammatory/anti-inflammatory mediators lipoprotein-associated phospholipase A2 and paraoxonase 1, respectively. Barnidipine should be mainly considered as an antihypertensive agent with neutral effects on most of the studied metabolic parameters in hypertensive patients. Any antioxidant effect of barnidipine needs further investigation.
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PMID:Effect of barnidipine on blood pressure and serum metabolic parameters in patients with essential hypertension: a pilot study. 1722 Apr 72

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