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)

Since several beta-blocking agents increase the atherogenic VLDL-triglycerides and decrease the atheroprotective HDL-cholesterol we studied if verapamil also affects these lipoproteins or the most atherogenic LDL-cholesterol. Twelve patients (three females), mean age 56 years, with angina pectoris or hypertension/tachyarrhythmias were treated with verapamil 240-320 mg/day. Serum lipoproteins were measured before and after 6 and 24 weeks of therapy. Initial total serum cholesterol averaged 7.27 mmol/l. After 6 weeks of treatment it decreased by 9%, p less than 0.02. These results remained significant, p less than 0.01 after 24 weeks. The decrease was due to a fall in LDL-cholesterol by 12%, p less than 0.01. The reduction in LDL-cholesterol was correlated to initial LDL-cholesterol concentration, r = -0.73, p less than 0.01. Within LDL there was a parallel decrease in phospholipids, p less than 0.05. There were no changes in total or VLDL-triglycerides or total HDL-cholesterol. In the HDL fraction HDL2 decreased insignificantly but HDL3 cholesterol increased by 12%, p less than 0.05. We conclude that verapamil has a beneficial effect on serum lipoproteins in that it lowers the atherogenic LDL-cholesterol and does not affect the other lipoproteins in an undesirable way.
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PMID:Effect of verapamil on serum lipoproteins in patients with angina pectoris. 658 55

Twenty patients receiving hemodialysis who had mild to moderate hypertension were treated with prazosin or propranolol to control predialysis hypertension. Effective blood pressure control was achieved with prazosin (mean dose 8.3 +/- 2.2 mg [+/- standard error of the mean], n = 10) and propranolol (mean dose 123 +/- 39 mg, n = 10). Therapy with prazosin did not significantly affect total plasma triglyceride or total cholesterol levels. The level of high-density lipoprotein (HDL) cholesterol tended to increase, but not significantly. However, the HDL3 subfraction did increase significantly, from 16.3 +/- 1.5 to 20.6 +/- 1.5 mg/dl (p = 0.05). Propranolol therapy increased plasma triglyceride levels, primarily of the very low density lipoprotein class. HDL cholesterol levels decreased from 44.2 +/- 6.7 to 34.7 +/- 4.2 mg/dl (p less than 0.03). The reduction in the HDL cholesterol levels was attributable to a decrease in HDL2 cholesterol levels (from 21.3 +/- 3.8 to 16.3 +/-3.0 mg/dl, p less than 0.04) and HDL3 cholesterol levels (from 23.0 +/- 3.1 to 19.5 +/- 2.1 mg/dl, difference not significant). Thus, both prazosin and propranolol are effective in controlling hypertension in patients undergoing hemodialysis. HDL3 cholesterol levels increased in patients treated with prazosin, but no other significant changes in the plasma lipids occurred. Patients treated with propranolol had a significant decrease in plasma HDL2 and HDL3 cholesterol levels.
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PMID:Effects of prazosin and propranolol on blood pressure and plasma lipids in patients undergoing chronic hemodialysis. 669 64

The effects of beta adrenoceptor blockade with propranolol or pindolol on serum total cholesterol, low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL), and its subfractions HDL2 and HDL3, serum triglyceride, and Intralipid clearance were studied in 17 normolipidaemic, non-diabetic patients with hypertension or angina pectoris. Both pindolol and propranolol had similar effects on fasting serum total and lipoprotein cholesterol concentrations. HDL2 cholesterol concentrations were reduced by 9 +/- 29% and HDL3 cholesterol increased by 11 +/- 16%, but there were no significant changes in total or LDL cholesterol in the combined groups after six weeks' treatment. After 12 weeks' treatment total cholesterol concentrations were reduced by 7 +/- 10% mainly owing to a reduction in the LDL fraction of 9 +/- 15%. Concentrations of HDL2 remained low, 8% less than control values. Serum triglyceride concentrations were increased by both drugs at six weeks but had returned to base values in the pindolol group by the twelfth week. Pindolol, but not propranolol, enhanced the rate of clearance of intravenous Intralipid.
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PMID:Effects of short term beta adrenoreceptor blockade on serum lipids and lipoproteins in patients with hypertension or coronary artery disease. 673 88

The effects of fluvastatin treatment on lipid profile and apolipoproteins were assessed in a group of 31 Chinese patients with hypercholesterolemia, maintained on a constant low-fat diet. Some patients had the additional cardiovascular risk factors of hypertension and non-insulin-dependent diabetes mellitus, and 6 patients had familial hypercholesterolemia. Baseline lipid levels were measured after a 4-week placebo period, and these were repeated after 4 weeks of treatment with fluvastatin 20 mg daily, and after 4 weeks of treatment with fluvastatin 40 mg daily. Total cholesterol, low density lipoprotein cholesterol, and apolipoprotein (apo) B were each reduced to the same extent with the 2 doses of fluvastatin (-20%, -26%, and -20%, respectively). Triglycerides and very low density lipoprotein cholesterol were also reduced by about 12% with the 2 doses of fluvastatin. Apo A-I was increased by 7% and high density lipoprotein cholesterol (HDL-C) was increased by 10% with the 40 mg dose. The increase in HDL-C was due to increases in both HDL2-C (18%) and HDL3-C (7%). Lipoprotein(a) levels did not show any significant change with the 2 doses of fluvastatin in this short-term study. One patient developed reversible asymptomatic elevation of liver enzymes with the higher dose of fluvastatin; otherwise the drug was well tolerated and no patients had to be withdrawn from the study.
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PMID:Effects of fluvastatin on lipid profile and apolipoproteins in Chinese patients with hypercholesterolemia. 760 89

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

We studied the heterogeneity of high-density lipoproteins (HDL) in plasma of 110 subjects, using three different methods: (a) gradient gel electrophoresis (GGE); (b) electroimmunoassay, to measure the concentration of lipoprotein particles containing apoprotein (apo) AI but no apo-AII (LP AI); and (c) cholesterol esterification rate (FERHDL) in very-low- and low-density lipoprotein-depleted plasma. There were two study groups: patients with hypertension, whose plasma lipid profile was similar to their respective controls, and patients with hypoalphalipoproteinemia (hypoalpha), whose family members served as controls. Values for FERHDL were significantly higher in both risk groups than in their respective controls. LP AI was significantly decreased only in the hypoalpha subjects. Generally, LP AI and FERHDL were inversely related. LP AI correlated strongly with plasma HDL-cholesterol, apo AI, and LP AI/AII; FERHDL correlated with those values inversely. LP AI, but not FERHDL, correlated with HDL free cholesterol. On the other hand, FERHDL correlated strongly with plasma concentrations of triglycerides and with the plasma ratio of total/HDL-cholesterol while LP AI did not. GGE determination of the composition of HDL subspecies showed that both FERHDL and LP AI were significantly related to the content of HDL2b particles: FERHDL inversely, LP AI directly; the relative amount of HDL3b,c particles correlated only with FERHDL. We conclude that GGE and FERHDL can be used to quantify both the apparently protective (HDL2b) and risk-associated (HDL3b,c) particles, whereas the concentration of LP AI in plasma mainly reflects the concentration of the HDL2 subpopulation.
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PMID:Structural and functional assessment of high-density lipoprotein heterogeneity. 788 38

Elevated insulin concentrations are frequently found in both men and women with coronary heart disease (CHD), and are likely to be due to insulin resistance. Hyperinsulinaemia may increase CHD risk by directly promoting atherogenesis, and insulin propeptides may also be important in this respect. However, increased insulin concentrations may adversely affect several other CHD risk factors, and it has been postulated that insulin resistance is a pivotal metabolic disturbance in a constellation of CHD risk factors. There is an association between hyperinsulinaemia and hypertension, although it is not known if this association is direct. Increased insulin concentrations are also associated with high triglycerides, low HDL or HDL2 concentrations, and increased small dense LDL. Obesity is also associated with insulin resistance, and it is the central or android body fat distribution which correlates with these metabolic disturbances. All these associated factors constitute a distinct syndrome--the insulin resistance syndrome--which is a frequent finding in patients with CHD, including microvascular angina. It is possible that the adverse associations of insulin resistance and dyslipidaemia are mediated through increased nonesterified fatty acid flux. Increased insulin levels are also associated with increases in the anti-fibrinolytic factor, plasminogen activator inhibitor-I (PAI-I). Whilst increased insulin levels are typically associated with insulin resistance, reduced hepatic insulin uptake may also be important. We now have techniques which can quantitate insulin secretion, hepatic uptake and release, elimination, and resistance. The menopause has appreciable effect on insulin and glucose metabolism. Estrogen and progesterone augment pancreatic insulin secretion, but the former reduces insulin resistance whilst the latter increases it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HRT mechanisms of action: carbohydrates. 819 41

The metabolic effects of captopril 25 mg twice daily and atenolol 50 mg daily on glucose, insulin and lipids were compared in 83 otherwise healthy mild-to-moderate hypertensive between the ages of 25 and 60 years in a randomised double-blind trial. Hourly glucose and insulin levels were measured during a 2-hour 75 g oral glucose tolerance test at baseline and after 12 weeks of treatment. Lipid profiles including total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, HDL2, HDL3, triglycerides, apoprotein (Apo)A1, ApoB, and Apo(a) were obtained before and after the treatment period. Blood pressure decreased significantly and equivalently in both treatment groups. The glucose and insulin levels and glucose x insulin product at 2 hours after the glucose load increased after 12 weeks of treatment with atenolol compared with the baseline values, but these parameters all decreased after the treatment period with captopril compared with their baseline values. These results indicate an improvement in insulin sensitivity with captopril and a deterioration with atenolol. HDL-cholesterol and HDL3 decreased in the atenolol group but increased in the captopril group. We conclude that captopril has more favourable effects than atenolol on glucose, insulin and lipid metabolism in the treatment of mild-to-moderate hypertension.
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PMID:A comparison of the metabolic effects of captopril and atenolol on glucose, insulin and lipoproteins in patients with mild-to-moderate essential hypertension. 860 Jun 7

The frequent coincidence of hypertension and dyslipidemia suggests that related genetic factors might underlie these common risk factors for cardiovascular disease. To investigate whether quantitative trait loci (QTLs) regulating lipid levels map to chromosomes known to contain genes regulating blood pressure, we used a genome scanning approach to map QTLs influencing cholesterol and phospholipid phenotypes in a large set of recombinant inbred strains and in congenic strains derived from the spontaneously hypertensive rat and normotensive Brown-Norway (BN.Lx) rat fed normal and high cholesterol diets. QTLs regulating lipid phenotypes were mapped by scanning the genome with 534 genetic markers. A significant relationship (P < 0.00006) was found between basal HDL2 cholesterol levels and the D19Mit2 marker on chromosome 19. Analysis of congenic strains of spontaneously hypertensive rat indicated that QTLs regulating postdietary lipid phenotypes exist also on chromosomes 8 and 20. Previous studies in the recombinant inbred and congenic strains have demonstrated the presence of blood pressure regulatory genes in corresponding segments of chromosomes 8, 19, and 20. These findings provide support for the hypothesis that blood pressure and certain lipid subfractions can be modulated by linked genes or perhaps even the same genes.
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PMID:Quantitative trait loci influencing cholesterol and phospholipid phenotypes map to chromosomes that contain genes regulating blood pressure in the spontaneously hypertensive rat. 869 78

Vascular cell membranes from patients with essential hypertension (EH) and animals with genetic forms of hypertension have been found to have alterations in the content of free cholesterol and negatively charged phospholipids that may modify their function. Since membrane and lipoprotein lipids exchange freely, the lipid composition of lipoproteins may be an indirect measure of the content of vascular and other cells. To determine whether abnormalities are present in the lipid and phospholipid composition of lipoproteins from patients with EH, 30 EH (11 women; 19 men) and 20 normotensive control subjects were studied. Since significant gender differences were present in a number of parameters of lipoprotein composition, male and female data were examined separately. The EH group of both sexes tended to have higher plasma TG and VLDL + LDL and HDL2 lipid levels than their respective controls. Not only were the calcium-binding phospholipids phosphatidylinositol (PI) + phosphatidylserine (PS), and the membrane fluidizer phosphatidylethanolamine (PE) were significantly reduced in their VLDL + LDL, but all phospholipids (L, sphingomyelin (SPH), PI + PS, and PE) were significantly reduced in their neutral lipid content in both the HDL2 and HDL3 subfractions. These directional changes in lipoprotein FC and phospholipid in the EH women significantly increased the EH FC/PC (mol/mol) ratio in their plasma, a new cardiovascular risk factor, (EH 1.08 +/- 0.22 vs. control 0.86 +/0 0.08; P < 0.01) and lowered the SPH/PC ratio HDL2 and HDL3 in EH patients of both sexes. These findings showed that lipoproteins in normolipidemic EH women are relatively enriched in FC and in EH patients of both sexes depleted in certain phospholipids lacking in lipoproteins, their functional properties could be altered and vascular tone increased.
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PMID:Abnormal lipoprotein phospholipid composition in patients with essential hypertension. 880 66


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