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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms of the changes in plasma lipids concentrations observed after beta-blockade were examined in 53 patients with hypertension receiving treatment with atenolol, metoprolol, propranolol, and oxprenolol in a randomised cross-over trial. Significant increases in mean plasma total and very-low-density lipoprotein (VLDL) triglyceride and reductions in high-density lipoprotein (HDL) cholesterol and free fatty acids concentrations wer observed with all four drugs, the increase in plasma triglyceride concentration being greatest after propranolol and oxprenolol. No significant changes were observed in total of LDL cholesterol concentrations, but HDL:LDL ratios and HDL cholesterol as a proportion of total cholesterol fell significantly. Thus plasma lipid concentrations should be monitored after three to six months of long-term treatment. Changes in triglyceride, HDL cholesterol and free fatty acid concentrations were associated with a highly significant reduction in clearance of soya oil (Intralipid) in 25 patients studied but were unrelated to changes in blood pressure. The fall in HDL cholesterol and rise in free fatty acid concentrations were significantly less in those with initially reduced HDL cholesterol or raised free fatty acid concentrations respectively. It is proposed that unopposed alpha stimulation inhibits lipoprotein lipase with a subsequent rise in plasma triglyceride and fall in HDL cholesterol concentration. Analysis of the relation between pretreatment concentrations and subsequent changes suggests that excessive alpha stimulation may impair production of HDL cholesterol in those with low HDL cholesterol concentrations before treatment. Subtle catecholamine-mediated changes in plasma lipid concentrations might provide a mechanism for the relation between stress and the development of cardiovascular events.
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PMID:Adrenergic mechanisms in control of plasma lipid concentrations. 612 83

It is certain that atherosclerosis is multi-factorial. Amongst the numerous risk factors two are particularly important: hypertension and primary or secondary abnormalities of plasma lipids and lipoproteins (high levels of total cholesterol, LDL and VLDL cholesterol, triglycerides or VLDL triglycerides, apoprotein B, low levels of HDL cholesterol, apoprotein A1 and probably HDL2). On the basis of a general review of the literature, the authors evaluate the changes in lipids, lipoproteins and apoproteins induced by different beta-blockers. Overall, the most constant and most obvious (particularly in hyperlipidaemic patients) disturbances combine an increase in total triglycerides or VLDL triglycerides and a fall in HDL cholesterol. There is little change in total cholesterol or LDL cholesterol. Side effects seen with most beta-blockers, cardioselective or not, differ in degree from one drug to another. They are particularly marked with some (propranolol) while they are virtually absent with others (pindolol). The mechanism of action is discussed (essentially inhibition of extra-hepatic lipoprotein lipase activity). These findings would seem to lead to the following practical conclusions: 1) Before starting antihypertensive treatment it is important to confirm lipid and lipoprotein levels, particularly bearing in mind the epidemiological links between moderate essential hypertension and lipoprotein abnormalities, especially those with a component of hypertriglyceridaemia. 2) Lipid profile including estimation by precipitation of HDL cholesterol must be studied during antihypertensive therapy and if there is a marked and confirmed deterioration towards an "increased atherogenicity", it is reasonable to envision a change of the antihypertensive agent. With the some efficacy on blood pressure levels and general tolerance, the choice should favour drugs having the least unfavourable effects on lipoprotein metabolism.
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PMID:[Changes in lipids and lipoproteins caused by the beta-blocking agents used as antihypertensives]. 613 67

Changes in aortic lipolytic enzyme activities (cholesterol esterase and lipoprotein lipase) and acid phosphatase activity during aging were investigated in three strains of rats with different blood pressures; stroke prone spontaneously hypertensive rats (SHRSP), spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKR). The blood pressures of male, 7 month old animals, was 234 (SHRSP), 173 (SHR) and 128 (WKR) mmHg. The cholesterol esterase activity markedly decreased with age in the aortas of SHRSP, SHR and normotensive WKR rats, while acid phosphatase activity decreased only slightly, if at all, and lipoprotein lipase activity remained unchanged. This effect was enhanced by increasing blood pressure in SHRSP, SHR and WKR. The total aortic cholesterol content increased significantly with hypertension in a inverse relation with cholesterol esterase activity. These results suggest that cholesterol deposition in aged arteries is, at least partialy, ascribable to an age-related decrease in cholesterol esterase, and that hypertension aggravates the deposition of arterial cholesterol by accelerating the age-related decrease in aortic cholesterol esterase activity.
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PMID:Age and blood pressure related changes in cholesterol esterase activity and cholesterol content in aortas of stroke prone spontaneously hypertensive rats, spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 742 53

Hypertensive patients are heavier and have a more centralized body fat distribution, which is associated with risk factor clustering and resistance to insulin's actions, including suppression of plasma nonesterified fatty acids. We postulated that abnormalities of nonesterified fatty acids contribute to the increased vascular alpha-adrenergic reactivity and tone observed in our previous studies of obese hypertensive subjects. To test this hypothesis, in two separate protocols 10% Intralipid was infused into a dorsal hand vein with heparin to activate lipoprotein lipase and raise fatty acid levels locally. In protocol 1, the effects of Intralipid/heparin compared with those of 5% dextrose/heparin on dorsal hand vein sensitivity to phenylephrine were assessed by use of the linear variable differential transformer technique in 8 normotensive subjects. In protocol 2, the effects of Intralipid/heparin were compared with those of saline/heparin on hand vein responses to both phenylephrine and angiotensin II in 11 normotensive African American women. Intralipid/heparin reduced the dose of phenylephrine required to produce 50% of the maximal venoconstrictor response from 582 to 137 ng/min (compared with dextrose/heparin, P < .01) in protocol 1 and from 293 to 137 ng/min (compared with saline/heparin, P < .01) in protocol 2. Intralipid/heparin did not significantly alter hand vein responses to angiotensin compared with saline/heparin. These data suggest that abnormalities of nonesterified fatty acids in obese hypertensive patients with risk factor clustering may contribute to their increased neurovascular tone.
Hypertension 1995 Apr
PMID:Fatty acids enhance vascular alpha-adrenergic sensitivity. 772 31

Arterial hypertension is frequently associated with serum lipid abnormalities. Lipid metabolism can also be affected by antihypertensive treatment, possibly via an interference with lipoprotein lipase (LPL) activity. The aims of this study were to investigate the metabolic and hemodynamic factors that can interfere with plasma postheparin LPL activity in a sample of 13 patients with mild, uncomplicated arterial hypertension. The effects of vasodilator administration (prazosin and hydralazine) alone or in combination with a beta-blocker (propranolol) were also studied. A direct correlation between serum insulin levels and LPL activity was found during placebo treatment. This was confirmed by multiple regression analysis, which also showed a positive correlation of LPL activity with aortic flow velocity and plasma adrenaline (F significance = 0.0007, R2 = .905). Serum insulin was also directly correlated with cholesterol in high-density lipoproteins (HDLs) and in the HDL2 subfraction. A significant decrease in LPL activity was observed during the addition of propranolol to vasodilators as compared with vasodilators alone. A positive correlation was found between LPL and adrenaline changes induced by the combined treatment. These data suggest that LPL may play a role in the pathophysiologic connections between insulin action, the adrenergic nervous system (ANS), and lipid metabolism.
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PMID:Factors affecting lipoprotein lipase in hypertensive patients. 778 54

Four points summarize the apparent major effects of selective alpha 1-inhibitors on lipid metabolism: stimulation of lipoprotein lipase; reduced VLDL synthesis and secretion; increase in the number of LDL receptors; and perhaps also a decrease in LDL cholesterol synthesis. Similar to the experimental data, the issues concern the type of patient, the clinical condition, normality, high cholesterol values or high triglyceride values, a combination of both, hypertension, and the degree of sympathetic activity.
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PMID:Lipid metabolism: implications of alpha 1-blockade. 790 Dec 43

The present study examined plasma lipoprotein, lipoprotein lipase, hepatic lipase, and insulin levels in men with borderline hypertension (diastolic blood pressure 85 to 94 mm Hg) compared with age-matched normotensive control subjects (diastolic blood pressure less than or equal to 80 mm Hg, n = 75 + 75). High-density lipoprotein (HDL) subclasses were determined in a subset (n = 45 + 45). While total and low-density lipoprotein cholesterol levels were similar, levels of very-low-density lipoprotein (VLDL) cholesterol and triglycerides (0.46 versus 0.41 mmol/L, P = .027, and 1.0 versus 0.85 mmol/L, P = .031) and total triglycerides (1.53 versus 1.33 mmol/L, P = .009) were elevated and HDL cholesterol was reduced in the borderline group compared with the normotensive group (1.17 versus 1.26 mmol/L, P = .043). The HDL subclass HDL2b concentration was lower (0.16 versus 0.24 mmol/L, P = .006), while HDL3b and HDL3c concentrations were higher in the borderline group (0.38 versus 0.32 mmol/L, P = .016, and 0.19 versus 0.16 mmol/L, P = .042). Significantly higher activities of hepatic lipase in the borderline group (282 versus 232 mU/mL, P = .024) and significant correlations between lipoprotein lipase activity and VLDL and HDL concentrations suggest an involvement of these enzymes in the development of these differences. When adjusted for body mass index or insulin level, all differences disappeared, except for HDL3b and HDL3c concentrations, which remained significantly elevated. These results indicate that dyslipoproteinemic changes are present in early hypertension. Although most of these changes are related to obesity, alterations in HDL profile were not explained by influences of body mass index and insulin.
Hypertension 1994 Nov
PMID:Dyslipoproteinemic changes in borderline hypertension. 796 21

Hypertriglyceridemia is a common feature of patients with increased blood pressure as well as several rodent models of hypertension. The goal of this study was to evaluate the effects of gemfibrozil on established abnormalities of triglyceride (TG) secretion and TG clearance in the Dahl salt-sensitive rat. Consequently, Dahl salt-sensitive rats received 12 days treatment with gemfibrozil (30 mg/kg/day) or vehicle by p.o. gavage and the following measurements were made: 1) fasting plasma TG levels; 2) TG secretion rate after suppression of TG removal with Triton WR 1339; 3) TG removal rate (half-time of disappearance of prelabeled very low density lipoprotein); and 4) lipoprotein lipase (LPL) activity and mRNA in soleus muscle, fat and liver tissues. Gemfibrozil produced a 50% reduction in fasting plasma TG concentrations, with no effect on TG secretion rate (17 +/- 2 vs. 15 +/- 1 mg/100 g b.wt./hr). The half-time of prelabeled very low density lipoprotein-TG removal was significantly lower in drug-treated animals (3.9 +/- 0.3 vs. 6.1 +/- 0.9 min), and this was associated with a tissue-specific increase in LPL activity in soleus muscle (153 +/- 5 vs. 135 +/- 5 U/g, P < .02). Expression of LPL mRNA, relative to beta-actin mRNA, was similar in both groups of rats. Thus, in this rodent model of hypertension and dyslipidemia, gemfibrozil lowers plasma TG levels by 50% with no effect on TG secretion; the hypotriglyceridemic effect is due mainly to an increase in TG removal rate associated with a post-transcriptional increase in LPL activity in skeletal muscle.
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PMID:Effects of gemfibrozil on triglyceride metabolism in Dahl salt-sensitive rats. 807 73

It has been reported that focal and segmental glomerulosclerosis (FSGS) with pronounced proteinuria rapidly develop in Dahl salt-sensitive hypertensive (DS) rats fed a high-salt diet. We found that even when they are fed a standard rat chow (0.3% NaCl), DS rats, especially males, exhibit marked proteinuria, hypoalbuminemia, and hypertriglyceridemia without marked hypertension at 32 to 38 weeks of age. The nephrosis was associated with spontaneously developed FSGS. We therefore investigated the mechanism of hypertriglyceridemia in nephrotic animals. Plasma triglyceride (TG) and apoprotein (apo) B levels were markedly increased in DS rats compared with Sprague-Dawley (SD) rats, and this was mainly attributable to an increase in the concentration of very-low-density lipoprotein (VLDL). The TG secretion rate estimated by the Triton WR1339 method was significantly greater in DS rats. VLDL-TGs isolated from both the DS and SD rats were endogenously radiolabeled with different isotopes, and a mixture of these was then injected into DS and SD recipients. The half-life of VLDL-TG was about three times longer in DS recipients, regardless of the source of VLDL. In SD recipients, VLDL from DS rats was cleared at a slower rate than VLDL from SD rats. The activity of lipoprotein lipase in postheparin plasma was substantially decreased in DS rats. Isoelectric focusing gel electrophoresis (IEF) showed that the ratio of apo E/C or apo C-II/C-III in VLDL was markedly decreased and the ratio of apo E or apo C to apo A1 in high-density lipoprotein (HDL) was slightly decreased in DS rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of hypertriglyceridemia in Dahl salt-sensitive rats, an animal model of spontaneous nephrotic syndrome. 812 10

The activity and mass of lipoprotein lipase (LPL) in postheparin plasma (PHP) from patients with hypertriglyceridemia coupled with hypertension, impaired glucose tolerance, hyperinsulinemia were investigated in order to clarify the cause of hypertriglyceridemia and the effects of bezafibrate (CAS 41859-67-0), a novel lipid lowering agent. Eight weeks of treatment with bezafibrate (200 mg/d) lowered plasma total cholesterol and triglyceride by 7 and 39%, respectively, and increased plasma high density lipoprotein (HDL) cholesterol by 23% in the patients (n = 15). The LPL activity and mass of PHP in the patients were found to be lower than in the normal controls. The LPL activity and mass of PHP in the patients before treatment with bezafibrate (n = 15) were 2.05 +/- 1.06 mumol/ml/h and 147 +/- 45 ng/ml, respectively, whereas after treatment with 200 mg/d of bezafibrate for 8 weeks, these values were 3.62 +/- 1.30 mumol/ml/h (p < 0.01) and 226 +/- 57 ng/ml (p < 0.05), respectively. The increases of LPL mass were positively correlated with the decrease of triglyceride levels during the same period. These results suggest that the expression of LPL enzyme protein is impaired in patients with hypertriglyceridemia coupled with hypertension, impaired glucose tolerance and hyperinsulinemia, and the impaired expression of LPL recovers during treatment with bezafibrate, resulting in improvement of hypertriglyceridemia.
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PMID:Effects of treatment with bezafibrate on lipoprotein lipase activity and mass in patients with hypertriglyceridemia. 814 47


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