Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relationships between plasma lipoproteins and cerebrovascular atherosclerosis are not completely clear. In a group of asymptomatic nondiabetic normolipidemic subjects, plasma lipid and apolipoprotein profiles have been related to extracranial carotid atherosclerotic lesions, as assessed by B-mode ultrasonography and independent relations between lipid and clinical parameters and carotid atherosclerosis have been evaluated. We have found that subjects with atherosclerotic lesions (both intimal thickening or plaque) had TG levels and CHO/HDL-C and LDL-C/HDL-C ratios significantly higher and HDL-C and apo A-I levels significantly lower in comparison with subjects with normal arteries. When patients were divided according to the lesions of carotid arteries subjects with atherosclerotic plaque presented HDL-C and apo A-I levels significantly reduced and TG and apo B levels and CHO/HDL-C and LDL-C/HDL-C ratios significantly increased in comparison with subjects with normal arteries, and HDL-C levels reduced and CHO/HDL-C and LDL-C/HDL-C ratios increased in comparison with subjects with intimal thickening. Patients with intimal thickening and normal subjects differed for HDL-C and TG levels and CHO/HDL-C and LDL-C/HDL-C ratios. At multivariate analysis HDL-C levels (negatively), age, hypertension and cigarette smoking (positively) resulted independently associated with cerebrovascular atherosclerosis. Our data seem to show that, although several lipid and apoprotein abnormalities are able to initiate the atherosclerotic process in extracranial carotid district, probably the presence of low HDL-cholesterol levels is an important condition to determine the further worsening of the lesions.
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PMID:Apo-lipoprotein profile in subjects with extracranial carotid atherosclerosis. 782 98

This study reports the changes in total cholesterol, triacylglycerols, apolipoproteins A-I, B, C-II and (a) before, directly after and 48 hours after chronic renal dialysis on 46 non-selected patients (20 male, 26 female; time since first dialysis 1-203 months (median 22 months), median age 52 years, range 25-82 years). Thirty six of the 46 patients (17 men and 19 women) suffered from hypertension. There were no sex-linked differences in any analyte except cholesterol, which was significantly higher in women than in men at all times. The apolipoproteins were determined with immunoluminometric assays. Apolipoprotein C-II was determined as the apolipoprotein C-II: apolipoprotein B complex. Lipoprotein(a) was determined using two antibodies directed against apolipoprotein(a). Significant increases (p < 0.05) in serum concentrations before and after dialysis were seen for all analytes with the exception of cholesterol (no significant change) and apolipoprotein C-II (significant decrease). The median increases were: cholesterol 5%, triacylglycerols 28%, apolipoprotein A-I 19%, apolipoprotein B 11%, apolipoprotein C-II -39%, lipoprotein(a) [all patients 21%, <300 mg/l 8%, > 300 mg/l 163%]. The values 48 hours after dialysis were not significantly different from the value before dialysis for cholesterol (-5%), apolipoprotein B (0%) and lipoprotein(a) (-2% - all patients). Statistically significant lower concentrations of apolipoprotein C-II (-28%) (p < 0.01) and triacylglycerols (-19%) (p < 0.01) were observed, but not investigated further. The behaviour of lipoprotein(a) was not correlated with any of the other analytes except triacylglycerols, where a statistically significant negative correlation was seen in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute changes in concentrations of apolipoproteins A-I, B, C-II and lipoprotein(a) in serum covering the period from directly before to 48 hours after chronic haemodialysis. 803 62

A randomized double-blind trial comparing the alpha-adrenergic blocker doxazosin and the beta-adrenergic blocker atenolol was completed by 131 patients with mild to moderate hypertension. Blood pressure and fasting blood lipids were determined at baseline and 4, 12, and 24 weeks of treatment. At entry, plasma lipids and lipoproteins were similar in those patients randomized to doxazosin or atenolol. After 24 weeks of treatment with atenolol, there were significant (P < .05) decreases in high-density lipoprotein cholesterol (HDL-C) and increases in triglycerides and very-low-density triglycerides (VLDL-T). In contrast, doxazosin was associated with significant (P < .05) increases in HDL-C and decreases in triglycerides and VLDL-T. There were no significant differences in HDL apolipoprotein (apo) A-I or low-density lipoprotein apoB between the drugs, but atenolol decreased the ratio of HDL-C to apoA-I, and doxazosin increased this ratio, differences that were statistically significant (P < .002). Neither apoA-I nor apoB concentration at baseline nor apoE phenotype was predictive of the lipid responses during antihypertensive treatment with either drug. Thus, there are significant favorable changes in HDL-C, total triglycerides, and VLDL-T between patients with mild to moderate hypertension and normal plasma lipids when treated with the alpha-blocker doxazosin compared with the beta-blocker atenolol. Plasma lipid or apo concentrations were not predictive of their lipid response during antihypertensive therapy with either of these agents.
Hypertension 1994 Aug
PMID:Lipids and lipoproteins during antihypertensive drug therapy. Comparison of doxazosin and atenolol in a randomized, double-blind trial: the Alpha Beta Canada Study. 803 50

Genetic variation at the apolipoprotein (apo) A-I/C-III/A-IV gene cluster on chromosome 11 has been associated with differences in occurrence of atherosclerosis and with variability in lipid levels among hypercholesterolemic-hypertriglyceridemic individuals. The functional cause of the association is not known, but polymorphisms of the apo A-IV gene are of interest because apo A-IV is involved in both triglyceride and cholesterol metabolism. Two mutations in the apo A-IV gene, 347T->S and 360Q->H, are known to cause amino acid substitutions in the mature protein. These polymorphisms were typed in a sample of 119 subjects with high cholesterol and high triglycerides in whom carotid artery wall thickness was previously shown to be strongly associated with silent polymorphic variation in the A-I/C-III/A-IV gene cluster. The relative allele frequencies were 0.83 and 0.17 for codon 347T->, and 0.95 and 0.05 for codon 360Q-> H. These polymorphisms did not show a statistically significant relationship with prevalent hypertension, diabetes, or cardiovascular disease or with plasma lipid levels. Most importantly, these amino acids substitutions in apo A-IV were not associated with carotid artery wall thickness. Therefore, the genetic cause of disease variability in a sample of mixed hyperlipidemics is not amino acid substitutions in codons 347 or 360 of the apoliproteins A-IV gene.
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PMID:No association of apolipoprotein A-IV codon 347 and 360 variation with atherosclerosis and lipid transport in a sample of mixed hyperlipidemics. 853 54

The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. Observations were made on the distribution of Lp(a), Lp(a) and other risk factors for cerebral infarction and these were statistically analyzed, primarily by multiple logistic regression analysis. The diagnosis of these cases was based on the Classification of Cerebrovascular Diseases III of the National Institute of Neurological Disorders and Stroke. The following results were obtained. 1) Lipoprotein (a) (1) Lp(a) did not show a normal distribution with the curve showing a gradual declining slope to the right. It was therefore considered not appropriate in our analysis to use as a means or standard deviation. (2) The 25th percentile, 50th percentile, and 75th percentile of the control group were 5.0 mg/dl, 11.0 mg/dl, and 22.4 mg/dl, respectively. In studying the distribution in these percentile ranges by subtypes of infarction, an increase in cases showing values greater than the median of the control group was observed in asymptomatic lacunar infarction, lacunar infarction, and atherothrombotic infarction, when compared to the control group. In asymptomatic lacunar infarction and lacunar infarction in particular, Lp(a) showed a significantly higher value compared to the control group. (3) However, by multiple logistic regression analysis to adjust for age and sex, Lp(a) did not show a significant odds ratio for asymptomatic lacunar infarction, lacunar infarction and atherothrombotic infarction. 2) Various serum lipids and other parameters (1) The various serum lipids did not show any involvement in asymptomatic lacunar infarction. However, involvement of HDLC and Apo A-I in lacunar infarction and atherothrombotic infarction was observed with the odds ratios in lacunar infarction being 4.2 with a confidence interval of 2.9-9.4 and 4.7 with a confidence interval of 2.2-10.1, and the odds ratios in atherothrombotic infarction being 3.1 with a confidence interval of 1.1-9.0 and 9.6 with a confidence interval of 3.0-30.5, respectively. (2) Involvement of diabetes mellitus in asymptomatic lacunar infarction and lacunar infarction was small, but a strong involvement in atherothrombotic infarction was observed with the odds ratio being 4.3 with a confidence interval of 1.2-16.2. (3) Involvement of hypertension in asymptomatic lacunar infarction and lacunar infarction was observed with the odds ratios being 2.6 with a confidence interval of 1.4-5.2 and 5.6 with a confidence interval of 2.4-13.0, respectively, but the involvement in atherothrombotic infarction was low. The foregoing results indicated that there was no involvement of Lp(a) as a risk factor for any type of cerebral infarction, unlike its involvement in coronary heart diseases. Only blood pressure was involved as a risk factor for asymptomatic lacunar infarction, but for lacunar infarction not only blood pressure but also HDLC and Apo A-I were involved as risk factors. HDLC, Apo A-I, and diabetes mellitus were involved as risk factors for atherothrombotic infarction, but the involvement of hypertension was minimal.
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PMID:Lipoprotein(a) and other risk factors for cerebral infarction. 856 15

Decreased response to vasopressor agents characterizes pregnancy. Endothelium-derived relaxing factors and vasodilating prostaglandins play an important role in the vascular tone during pregnancy. Since inhibition of nitric oxide (NO) biosynthesis induced by NO2-arginine enriched diet produced hypertension we measured in vivo cardiovascular responses to PGF2 alpha, L-arginine (L-arg) and cicletanine (Cic, IPSEN, France) which enhances PGI2 production. From day 13 to day 20 of gestation 4 groups of female Wistar rats were fed NO2-arg (31 mg/kg/d), NO2-arg+Cic (10 mg/kg/d), Cic enriched or control diet (C). Mean arterial pressure (MAP) was measured via a carotid catheter in anesthetized rats. Injection of PGF2 alpha (50 micrograms/kg) in jugular vein significantly increased MAP in the NO2-arg group versus, NO2-arg+Cic, Cic and C group (+23.5 +/- 3.3 vs +15.7 +/- 2.2, +15.8 +/- 2.2 and +17 +/- 1.85 mmHg; p < 0.01). Injection of L-arg (100 mg/kg) or Cic (1 mg/kg) 5 min before PGF2 alpha produced no modification in MAP in C and Cic group. Likewise in NO2-arg group injection of L-arg or Cic produced a diminished pressor response to PGF2 alpha (+23.5 +/- 3.3 vs -17.5 +/- 1.7 mmHg; p < 0.05 and +15.2 +/- 2.4 mmHg; p < 0.01 respectively). In NO2-arg+Cic group, only injection of Cic induced a diminished pressor response to PGF2 alpha which is more important without L-arg (+15.7 +/- 2.2 vs +9.1 +/- 1.3 mmHg; p < 0.001) or with L-arg (+13.6 +/- 1.5 vs +9.1 +/- 1.3 mmHg; p < 0.01). Cicletanine also significantly diminished the proteinuria in the NO2-arg+Cic group versus NO2-arg group (13.9 +/- 4.36 vs 63.4 +/- 21.6 mmHg; p < 0.01). IN CONCLUSION, chronic NO synthesis inhibition enhanced blood pressure and pressor responses to PGF2 alpha during pregnancy in rats. Chronic administration of cicletanine in Wistar pregnant rats decreases the response to vasopressor agents like PGF2 alpha. Moreover acute and chronic administration of cicletanine blunted the pressor effect, which was lower than in normal gestation.
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PMID:[Chronic and acute effect of cycletanine in NO-dependent hypertensive pregnant rats]. 857 78

Nitric oxide (NO) synthesis is induced in glomeruli in glomerulonephritis; its role in the pathogenesis of glomerular injury is unknown. Interpretation of its role using the currently available analogues of L-arginine as in vivo inhibitors of NO is complicated by their lack of specificity for inducible NO synthase (iNOS). As NO synthesis by iNOS depends on extracellular L-arginine, we have here examined effects of L-arginine depletion on glomerular NO synthesis and the course of accelerated nephrotoxic nephritis (NTN). Arginase, which converts L-arginine to urea and L-ornithine, was used to achieve L-arginine depletion. A single dose of i.v. arginase produced complete depletion of plasma arginine for four hours. Two forms of NTN were induced in preimmunised rats by nephrotoxic globulin: (1) the systemic form of the model by intravenous nephrotoxic globulin; or (2) the unilateral form of model by left kidney perfusion with nephrotoxic globulin, which avoids the complications of systemic administration of nephrotoxic globulin. Arginase reduced plasma arginine levels and the synthesis of nitrite (the stable end-product of NO) by NTN glomeruli (95% inhibition). Proteinuria was exacerbated. There was no effect on early (24 hr) leukocyte infiltration. In the systemic form of the model arginine depletion by i.v. arginase increased glomerular thrombosis at 24 hours, and the severity of histological changes at four days, accompanied by systemic hypertension. In the unilateral form of the model, where i.v. arginase did not induce hypertension, there was no increase in thrombosis or histological severity of nephritis. These results show that arginine depletion, which inhibits glomerular NO synthesis in NTN, leads to increased proteinuria. Where injury is severe, or accompanied by systemic hypertension, the disease is further exacerbated by glomerular thrombosis. These results suggest that NO has an important role in limiting acute glomerular injury.
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PMID:L-arginine depletion inhibits glomerular nitric oxide synthesis and exacerbates rat nephrotoxic nephritis. 869 29

The objective of this study was to assess the medium-term effects of betaxolol, a long-acting, lipid-soluble, cardioselective, beta-adrenergic antagonist, alone and in combination with nitrendipine on blood pressure (BP) and metabolism of lipid, lipoprotein and apolipoprotein in patients with mild to moderate hypertension. Forty-seven patients (21 men, 26 women, average age 54 years) participated in an open controlled clinical trial. After a 4-week washout period, all of the patients received betaxolol monotherapy at a dose of 5-10 mg daily for 6 months (Phase I). From month 7 through month 12 (Phase II), half of the total patients (Group B, n = 23) with diastolic blood pressure (DBP) of 95 mm Hg or more at the end of Phase I were also given nitrendipine (10-20 mg, once daily), while the remaining patients (Group A, n = 24) continued to receive only betaxolol. Systolic blood pressure (SBP), DBP, and heart rate (HR) were monitored once monthly. Serum lipid profiles were measured at study entry and after 6 and 12 months of therapy. Betaxolol significantly reduced SBP, DBP, and HR in both groups during Phase I, and the reductions in SBP and DBP were markedly less in Group B than in Group A. During Phase II, the additional reduction of SBP and DBP to levels similar to those in Group A was achieved by betaxolol in combination with nitrendipine, and HR was slightly but significantly increased. Betaxolol monotherapy reduced serum levels of high density lipoprotein cholesterol (HDL-C) and increased levels of triglyceride, apolipoprotein (apo) C-II and apo C-III. Combination therapy with betaxolol and nitrendipine increased serum apo A-I but did not affect other lipid profiles. Our results indicate that betaxolol is an effective antihypertensive drug which has a preferable effect on HR and HDL profiles when combined with nitrendipine.
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PMID:Medium-term effects of betaxolol monotherapy and combination therapy with nitrendipine on lipoprotein and apolipoprotein metabolism in patients with mild to moderate essential hypertension. 873 59

The objective of this study was to determine whether phenolic constituents present in red wine and grape juice modulate plasma lipid and lipoprotein concentrations in healthy human subjects. All subjects consumed in random order 375 ml of red or white wine per day or 500 ml of two different grape juices (high and low phenols) per day for periods of 4 weeks separated by 2-week periods of abstention while continuing normal activity and food intake, and their normal lives in a community setting. The subjects were 24 healthy males aged 26-45 years screened by clinical examination and laboratory tests to exclude hypertension, diabetes mellitus, hyperlipidemia and obesity, among others. Fasting blood was collected at the beginning and end of each beverage schedule for analysis of lipids and lipoproteins. Changes in plasma lipids and lipoproteins in response to each beverage were measured to determine whether these were altered by red wine and grape juice phenolics independently of the effects of ethanol. Both grape juices had virtually no effect. Red and white wines raised plasma HDL-cholesterol and apo A-I and apo A-II concentrations as well as the apo A-I:apo B ratio to a similar extent. Red wine also raised plasma triglyceride and total cholesterol concentrations. Neither wine affected plasma apo B or apo (a) concentrations. The favourable effects of wines in modulating plasma lipid and lipoprotein concentrations are probably due to their alcohol content and cannot be reproduced by grape juices.
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PMID:Wine: does the colour count? 881 66

Increased body weight has been associated with an increased risk of morbidity and mortality from coronary heart disease (CHD) in several populations. We studied the distribution of body mass index (BMI, kg/m2) in men (n = 1566; mean age, 49 +/- 10 years) and women (n = 1627; mean age, 49 +/- 10 years) participating in the third examination cycle of the Framingham Offspring Study and the association of BMI with known CHD risk factors. In men, BMI increased with age until age 50 years, when it reached a plateau. In women, there was a trend toward an increase in BMI with age up to the seventh decade of life. Seventy-two percent of men and 42% of women had a BMI > or = 25.00, the cutoff point for the definition of overweight. In age-adjusted analyses, BMI was significantly and linearly associated with systolic blood pressure, fasting glucose levels, plasma total cholesterol, VLDL cholesterol, and LDL cholesterol levels and was inversely and linearly associated with HDL cholesterol levels (P < .001) in nonsmoking men and women. The association between BMI and apolipoprotein B and A-I was similar to that of LDL and HDL cholesterol, respectively. LDL size was also linearly associated with BMI: subjects with higher BMI had smaller LDL particles. Lipoprotein(a) levels were not associated with BMI in this population. Of all these risk factors for CHD, reduced HDL cholesterol levels and hypertension were those more strongly associated with higher BMI in both men and women. Elevated triglyceride levels and small LDL particles, and diabetes in women, were also strongly associated with higher BMI values in this population. Our results indicate that a high prevalence of adult Americans are overweight and support the concept that increased BMI is associated with an adverse effect on all major CHD risk factors. These results emphasize the importance of excess body fat as a public health issue.
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PMID:Impact of body mass index on coronary heart disease risk factors in men and women. The Framingham Offspring Study. 897 56


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