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)

During a double-blind, randomized study in hypertensive patients, changes in blood pressure (BP) and in plasma lipid and lipoprotein levels during treatment with celiprolol were compared with those occurring during nifedipine treatment. Fifty-three patients (28 men and 25 women) with mild-to-moderate hypertension, aged 20-64 years, were studied. After a 1-month placebo run-in period, patients were randomly assigned to receive either nifedipine (40 mg daily) or celiprolol (200 mg daily) each time using a double dummy technique. After 6 weeks, dosages of each drug could be doubled. Both drugs caused similar reductions in blood pressure but after 12 weeks treatment, the percentage of decrease in diastolic BP (DBP) was more pronounced (p less than 0.01) in the nifedipine group (-18%) than in the celiprolol group (-12%). After 6 weeks, there were no differences in plasma lipids between the two treatment groups. However, the changes after 12 weeks treatment were different (p less than 0.05) between the groups, leading to lower levels of plasma esterified cholesterol, low-density lipoprotein (LDL) cholesterol and apoprotein AI, AII, and B in the celiprolol group. Plasma lecithin cholesterol acyltransferase activity (LCAT) was not modified, suggesting that reverse cholesterol transport was not affected by the drugs. In both treatment groups, a significant positive relationship was observed between changes in LDL cholesterol and apoprotein B. As compared with nifedipine, celiprolol after 12-week therapy had a rather favorable plasma lipid profile. The clinical relevance of such findings, in terms of prevention of cardiovascular complications, has yet to be established.
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PMID:Comparison of the effect of celiprolol and nifedipine on blood pressure and plasma lipids. 138 Oct 18

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
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PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

The purpose of this study was to investigate the effect of carvedilol on serum lipids in patients with mild-to-moderate essential hypertension. Twenty-one patients with blood pressure greater than or equal to 160/95 mm Hg after a 4-week placebo run-in period were initially given 10 mg of carvedilol once daily. The dose was increased to 20 mg after 4 weeks if the target blood pressure was not achieved. The duration of treatment was 12 weeks. After 12 weeks of administration, blood pressure and the pulse rate (PR) declined significantly (blood pressure from 173/105 to 142/91 mm Hg, p less than 0.001; PR from 74 to 67 beats/min, p less than 0.001); however, serum lipids [total cholesterol, triglycerides, low-density lipoprotein, high-density lipoprotein (HDL), HDL2, and HDL3], lipoprotein fraction (alpha, pre-beta, and beta), apoprotein fraction (A-I, A-II, CII, CIII, and E), and atherogenic index [(total cholesterol - HDL cholesterol) divided by HDL cholesterol] were not altered significantly. There were no side effects reported during the trial. From these results, it can be concluded that carvedilol has no adverse effect on the coronary risk profile as reflected by lipid measurements, and is an efficacious, safe, well-tolerated antihypertensive drug in patients with mild-to-moderate hypertension.
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PMID:Effects of carvedilol on serum lipids in patients with essential hypertension. 172 79

By cholesterol feeding, atherogenic VLDL, beta-VLDL (IDL) and LDL increased more remarkably in SHRSP than in normotensive WKY, suggesting that hypertension may promote the productions of atherogenic lipoproteins. On the other hand, HDL significantly decreased in SHRSP, which was associated with the decrease in apoA-I and E in the HDL fraction. This indicates the decreases of two HDL subfractions, apoE HDL and apoA-I HDL, in SHRSP. These decreases of HDL subfractions in SHRSP may be closely related to the higher h-TGL activity in SHRSP than in WKY, and could be a trigger of the excess production of atherogenic lipoproteins.
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PMID:Effect of cholesterol feeding on the compositions of plasma lipoproteins and plasma lipolytic activities in SHRSP. 177 30

Atherosclerosis is the main cause of mortality in diabetic patients, and the incidence of coronary heart disease is increased in the presence of microalbuminuria. The mechanisms of this association are not known and could involve genetic factors (predisposition to hypertension), renal disease and dyslipidemia. An increase in plasma triglyceride and apoprotein B levels, a decrease in plasma HDL cholesterol, qualitative abnormalities of VLDL and HDL are related to cardiovascular risk in diabetic patients. All these factors are worsened by nephropathy. Lipoproteins abnormalities could be involved in the progression of renal injury. In microalbuminuric patients, it seems important to reduce glomerular hyperfiltration and to normalize glycemia and blood pressure in order to prevent impairment of renal injury and dyslipidemia induced by nephropathy. Early treatment of lipoprotein abnormalities could decrease the incidence of cardiovascular complications.
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PMID:[Association of atherosclerosis and nephropathy in diabetes mellitus. Role of lipid anomalies]. 183 72

Hyperinsulinaemia is said to be a risk factor for cardiovascular disease, but the extent to which different insulinaemic measures are associated with vascular risk factors in ostensibly healthy individuals, and whether they operate independently in men and women, remains uncertain. The association between risk factors and various insulinaemic measures was examined in 148 men and 118 women who were normoglycaemic, normotensive, and non-obese (body mass index in men less than 27, in women less than 25). A 75 g glucose tolerance test was administered after blood sampling for fibrinogen, lipids, lipoproteins and insulin. Insulin was also measured after 1 and 2 hours. Significant univariate correlations (p less than 0.01) were most consistently recorded between insulinaemic measures and fasting serum triglycerides in men and women, whilst systolic blood pressure only correlated with insulinaemia in women, and diastolic blood pressure correlated with fasting and 2 hour insulinaemic measures in men and women. Inconsistent associations were noted with total serum cholesterol in men and women, with high density lipoprotein cholesterol, body mass index, apoprotein B and A1 in men, and with fibrinogen in women. Age was not correlated with any insulinaemic measure in men or women. Differences in vascular risk factors between quintiles of the insulinaemic measures were examined, after correction for body mass index. The dominant association with fasting and post-glucose load insulinaemic measures was with triglycerides, especially in women, with less frequent graded differences between quintiles observed for total cholesterol, and diastolic and systolic blood pressures in men and women. The incidence of other risk factors often only differed in the lowest or highest quintile in comparison to other quintiles, suggesting a threshold rather than a graded effect. Furthermore, differences in HDL cholesterol and apoprotein B were only recorded for top quintiles of post-glucose challenge/integrated insulinaemic measures in men, whilst serum fibrinogen concentrations only differed significantly in women in the top insulinaemic area under the curve quintile. In the absence of additional risk factors such as diabetes, hypertension and obesity, insulinaemic measures are not consistently related to blood pressure and measures of lipid metabolism and coagulation, and are thus a weak predictor of other cardiovascular risk factors. The vascular risk profile associated with insulin appears somewhat different in apparently healthy men and women.
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PMID:The association of different measures of insulinaemia with vascular risk factors in healthy normoglycaemic normotensive non-obese men and women. 194 34

To determine the influence of the apolipoprotein E polymorphism on the occurrence of coronary artery disease (CAD) and on serum lipids, lipoproteins and apolipoproteins we studied 145 patients with angiographically defined CAD and compared them with 153 control subjects without history or complaints of vascular disease and with 35 subjects without significant stenosis on coronary arteriography. Subjects with hypertension, diabetes mellitus and endocrine or metabolic disorders were excluded. Covariance analysis and logistic regression analysis were performed with adjustment for age, sex, smoking habits and relative body weight. There were no significant differences for the apoE phenotypes on risk of cardiovascular disease. The CAD group had significantly higher mean values of serum cholesterol and triglycerides, very-low-density lipoprotein (VLDL)-cholesterol and VLDL-triglycerides, low-density lipoprotein (LDL)-cholesterol and apoprotein B; they had lower high-density lipoprotein (HDL)-cholesterol and apo A-I. The combination of LDL-cholesterol, apoA-I and VLDL-cholesterol was the best model in predicting cardiovascular disease. ApoE phenotype group E3/E2 had significantly lower values for serum cholesterol, LDL-cholesterol, and apoB and higher levels of apoE in comparison with the phenotype groups E3/E3 and E4/E3. The combination of LDL-cholesterol, cholesterol, apoE and VLDL-triglycerides was the best model in predicting the apoE phenotype. Thus, taking other risk factors into account, the apoE phenotype is not an independent risk factor for CAD; the apoE polymorphism influences lipoprotein levels and possibly, in that way, indirectly also the risk for CAD.
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PMID:Apolipoprotein E phenotypes, serum lipoproteins and apolipoproteins in angiographically assessed coronary heart disease. 194 27

The purpose of the present study was to evaluate the influence of obesity on ischaemic heart disease frequency in a well-documented type II diabetic population. To eliminate one of the possible sources of variability for plasma lipid concentrations, only subjects showing the apoprotein E phenotype, indicative of homozygosity for the epsilon 3 allele (i.e. an E3/E3 genotype), have been recruited. A larger prevalence of ischaemic heart disease was noticed among obese patients as compared to non-obese or merely overweight subjects according to a higher frequency of hypertension and to higher triglyceride concentrations. These results corroborate the hypothesis of a common pathogenesis of the major cardiovascular risk factors.
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PMID:Relationships between obesity and ischaemic heart disease in type II diabetic subjects homozygous for the apoprotein E3 allele. 195 96

For the past 40 years, adrenoreceptors have been studied as the biomolecular mediators of tissue response to catecholamines. An expanded role of alpha-adrenoreceptors in the regulation of risk factors for coronary heart disease (CHD) has recently emerged. Hypercholesterolaemia, hypertension, and cigarette smoking are the major risk factors and their interactions are associated with increased mortality. Control of hypertension alone has failed to reduce the risk of CHD. Conversely, reduction of elevated total cholesterol and low density lipoprotein (LDL)-cholesterol has been shown to lower the risk of CHD. As a result, multiple risk factor approaches to the management of patients have evolved in attempts to reduce deaths from CHD. Selective alpha 1-adrenoreceptor antagonists appear to have a dual function in CHD risk management since they control elevated blood pressure by peripheral vasodilatation and reduce atherogenic lipids by several mechanisms. With selective alpha 1-blockade, the number of LDL-cholesterol receptors is up-regulated and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG Co-A reductase) activity is suppressed causing reductions in total cholesterol, LDL-cholesterol, and apoprotein B levels. Effects on intermediary metabolism reduce synthesis of very low density lipoprotein (VLDL) which contributes to a reduction of total triglyceride levels and, to a lesser extent, to a reduction of total cholesterol levels. Increased lipoprotein lipase activity leads to reduced total triglyceride and VLDL levels and to increased high density lipoprotein (HDL)-cholesterol levels. As demonstrated by the initial prospective data from Phase I of the Treatment of Mild Hypertension Study (TOMHS), both reduction of raised blood pressure and beneficial lipid modifications are sustained (1 year) with selective alpha 1-blockade. The prospective benefits on morbidity and mortality from CHD of such favourable changes in these two major risk factors remain to be quantified.
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PMID:Alpha 1-adrenoreceptor blockade and the molecular basis of lipid metabolism alterations. 197 19

Hyperglycaemia, a raised fibrinogen, an increased serum triglyceride and a reduced HDL-cholesterol are common metabolic features of non-insulin dependent diabetes mellitus (NIDDM). Hypertension is frequently associated with NIDDM, however the influence of antihypertensive therapy on these combined factors in the diabetic is at present unclear. In a double-blind placebo-controlled crossover study in 20 stable NIDDM subjects with hypertension, the metabolic effects of 6 weeks' treatment with the alpha-blocker, doxazosin, was compared with treatment with the beta-blocker, atenolol. Similar and significant reductions in BP were produced by both drugs. Significant increases in weight, HbA1, apoprotein B, serum triglyceride and cholesterol/HDL ratio were observed with atenolol therapy. Doxazosin therapy was associated with opposite patterns of changes in fasting glucose, lipids and lipoproteins but only for serum triglyceride was difference between treatments significant. Fibrinogen was not altered by either treatment. Conclusions from this study indicate; 1) adrenergic mechanisms may be an important influence on glucose homeostasis and lipid metabolism in NIDDM and 2) the beta-blocker, atenolol, has a small adverse effect on weight, glycaemic control and the atherogenic lipid profile, whereas the alpha-blocker, doxazosin, has no such effect and may, in part, correct the disturbances of lipoprotein metabolism characteristic of NIDDM.
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PMID:Alpha-blocker therapy; a possible advance in the treatment of diabetic hypertension--results of a cross-over study of doxazosin and atenolol monotherapy in hypertensive non-insulin dependent diabetic subjects. 198 Sep 30


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