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

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

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

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

Previous studies have indicated that in HepG2 cells HDL3-signalling involves glycosylphosphatidylinositol (GPI) anchored proteins. HDL3-binding to HepG2 cells was found to be enhanced by cellular preincubation with PI-PLC inhibitors and sensitive to a cellular preincubation with exogenous PI-PLC, suggesting that HDL3 binds directly on GPI-anchored proteins to initiate signaling. Moreover HDL3-binding was found to be partly inhibited by antibodies against the HDL-binding protein (AbHBP). HDL3, when binding to HepG2 cells, promoted the release in the culture medium of a 110 kDa protein that binds AbHBP, while a cellular preincubation with antibodies against the inositol-phosphoglycan (IPG) moiety of GPI-anchor (AbIPG), used to block lipolytic cleavage of the GPI-anchor, inhibits HDL3-induced release of the 110 kDa protein in the culture medium. In [3H]-PC prelabeled HepG2 cells, AbHBP were found to stimulate PC-hydrolysis and DAG generation within 5 min as did HDL3 stimulation. Cellular preincubation with AbIPG was found to inhibit only the HDL3-signal and not the AbHBP-signal, while a prior cellular pretreatment with PI-PLC from Bacillus cereus was found to inhibit the HDL3-and AbHBP-signal. Moreover cellular preincubation with AbHBP for 1 h at 37 degrees C was found to inhibit HDL3-signalling pathways. Our results suggest that in HepG2 cells a 110 kDa protein, which could be HBP, can be anchored to the membrane via GPI, and can function in HDL3-signalling pathways as binding sites.
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PMID:HDL3 binds to glycosylphosphatidylinositol-anchored proteins to activate signalling pathways. 929 27

The aim of the study was the estimation of the lipid profile and prevalence of dyslipoproteinemia in patients with essential hypertension. The study group consisted of 108 outpatients (61 men and 47 women) with mild to moderate hypertension (HT), aged 35-64, who did not receive antihypertensive drugs for at least four weeks. The matched controls (MC) were randomly chosen for each HT patient from population of Warsaw inhabitants, covered by Pol-MONICA II screen. The concentrations of total cholesterol (CH) and triglycerides (TG) in serum and cholesterol in lipoprotein fractions and subfractions (LDL, HDL, HDL3) were measured by enzymatic methods. The levels of apolipoproteins (Apo A-I, Apo B) were estimated by immunoassay. Laboratory was under control of WHO-Lipid Reference Laboratory and CDC-NHLBI Lipid Standardization Program. In HT the concentration of cholesterol in LDL was significantly higher (p < 0.001) than in MC, both in men (by 15%) and in women (by 22%), but the concentrations of cholesterol in HDL and HDL3 and Apo A-I (in men only) were significantly lower (p < 0.001) in HT than in MC in men (by 21% and by 26%) as well in women (by 16% and by 25%). Also in HT group the mean levels of TG, CH and Apo B were higher than in MC, but these differences were significant only in TG level in men. In HT group the prevalence of normolipemia was twice lower than in MC (22% and 42%). Essential hypertension fractions is associated with abnormal levels of some lipoprotein fraction and with higher prevalence of hyperlipoproteinemia. The coexistence of both abnormalities may be particularly detrimental as important factor in the development of atherosclerosis.
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PMID:[Dyslipoproteinemia in primary hypertension]. 931 61

To study the relationship of the concentration of serum lipoprotein (a) [Lp(a)] with diabetic complications in non-insulin dependent diabetes mellitus (NIDDM), 100 non-diabetics with 150 patients with NIDDM were compared. There was no difference in Lp(a) concentration (P > 0.5) between the two groups. Lp(a) concentration was not significantly correlated with the levels of total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, apolipoprotein A-I, apolipoprotein B in both groups. In NIDDM group, patients with hypertension, macro- and microangiopathy had higher levels of Lp(a) than those without these complications (P < 0.001 and P = 0.002 respectively). Lp(a) level was positively related to presence of macroangiopathy (r = 0.185, P = 0.024) and proteinuria (r = 0.316, P < 0.001) in NIDDM.
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PMID:[Lipoprotein (a) and non-insulin dependent diabetes mellitus]. 938 40

Adhesion molecules on the endothelial cell membrane play an important role in the pathogenesis of atherosclerosis. Levels of soluble forms of cell adhesion molecules are reportedly elevated in patients with peripheral artery vessel disease and in patients with an atherosclerotic aorta. The present study investigated the association of serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble intercellular adhesion molecule 1 (sICAM-1), and soluble P-selectin (sP-selectin) with coronary heart disease (CHD) and the extent of coronary atherosclerosis, and examined the influence of serum levels of lipids, lipoproteins and apolipoproteins (apo) in subjects with (n=52, M/F:43/9) and without (controls, n=40, M/F:25/15) angiographically proven coronary atherosclerosis. After controlling for age and gender, levels of sVCAM-1 (least squares mean +/- std error: 565+/-36 ng/ml vs 540+/-41 ng/ml, ns), sICAM-1 (261+/-17ng/ml vs 247+/-19ng/ml, ns), and sP-selectin (142+/-8ng/ml vs 149+/-10 ng/ml, ns) in patients with coronary atherosclerosis were not different from those in controls, as assessed by an analysis of covariance. After also adjusting for body mass index, hypertension, diabetes mellitus, and smoking by a multiple logistic function analysis, the association of sVCAM-1, sICAM-1, and sP-selectin with CHD was still not significant. Levels of sVCAM-1, sICAM-1, and sP-selectin were also not related to the extent of coronary atherosclerosis as judged by the number of stenosed vessels. However, inverse (p<0.05) relationships were observed between sVCAMs and serum levels of HDL3-cholesterol, apo A-II, and lipoprotein containing apo A-I and A-II, between sICAMs and levels of apo A-II and Lp A-I/A-II (Lp A-I/A-II), and between sP-selectin and lipoprotein containing only apo A-I. In conclusion, serum levels of soluble VCAM-1, ICAM-1, and P-selectin were not related to CHD or the extent of coronary atherosclerosis, but were inversely related to serum levels of high-density lipoprotein-related lipoproteins.
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PMID:Levels of soluble cell adhesion molecules in patients with angiographically defined coronary atherosclerosis. 1008 83

Contents of 7 serum lipoprotein (LP) fractions both native and after their incubation under 37 degrees C during 24 h in the patients with atherosclerosis and hypertension discirculatory encephalopathy were investigated by a gradient gel-electrophoresis method. Two groups of patients in the age of 30-59 in the first group and 61-73 in the second one were examined. It was found that for the age interval examined in native serum of the patients with atherosclerosis and hypertension similar changes of LP contents were observed. These changes were expressed a increasing apoA- and decreasing apoB-containing LP fractions as compared with the control. After the temperature incubation of healthy persons serum the amount of LDL increases and amount of HDL3 declines. The latter is a result of LP lypolysis and etherification normal processes. On the base of the data obtained we may suppose that in the patients with hypertension these processes also have some aged peculiarities, although less intensive as compared with the healthy persons. In contrast to the latter after the temperature incubation of serum (in vitro) in the patients with atherosclerosis there were no any statistically significant changes of any LP fractions contents that may evidence about depression of LP transformation in the isolated serum in such patients.
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PMID:[Serum lipoproteins in elderly patients with cerebrovascular pathology]. 1203 8

Treatment of hypertension with beta-adrenergic blockers (BB) slightly increases plasma triglycerides and decreases high density lipoprotein (HDL) cholesterol levels. However, only little is known about BB-related lipid changes in patients with coronary artery disease (CAD), who usually a priori have decreased HDL cholesterol levels; and even less data exist on HDL subfraction cholesterol in these patients. We therefore quantified levels of lipids, lipoprotein lipids including HDL2 and HDL3 cholesterol, and apolipoproteins in 107 consecutive men undergoing elective coronary angiography. Of the 107 patients, 84 had angiographically established coronary atherosclerosis (>or=1 lesion with >or=50% narrowing, CAD+), and 23 had no major lesion (CAD-); 67 were taking ss1-selective BB (metoprolol or atenolol) for treatment of angina and/or hypertension and 40 were not. Patients using BB had significantly higher cholesterol levels than patients not using BB (5.99 +/- 0.93 vs. 5.63 +/- 1.07 mmol/l, mean +/- SD, p = 0.029). Their HDL cholesterol and HDL2 cholesterol levels were significantly lower (1.19 +/- 0.27 vs. 1.28 +/- 0.33 mmol/l, p = 0.048, and 0.22 +/- 0.12 vs. 0.27 +/- 0.18 mmol/l, p = 0.038, respectively). Accordingly, the total cholesterol/HDL cholesterol ratio was significantly higher in patients taking BB than in those not taking BB (5.23 +/- 1.27 vs. 4.68 +/- 1.63, p = 0.010). Considering CAD+ and CAD- patients separately, there was a trend towards lower HDL cholesterol and its subfractions with significantly lower HDL2 cholesterol in patients with BB in the CAD- group, suggesting a stronger dyslipidemic effect of BB in these patients with a priori normal or near normal baseline lipid levels.
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PMID:High density-lipoprotein subfractions of patients using cardio-selective beta-blockers. 1209 Sep 5

The metabolic syndrome and type 2 diabetes are associated with endothelial activation (and thus with inflammatory processes leading to atherosclerosis), but the mechanisms that underlie these associations are not fully understood. Endothelial intercellular adhesion molecule (ICAM)-1 plays an important role in the recruitment of immune cells during the development of atherosclerotic plaque and is a marker of inflammatory disease. We performed bivariate quantitative genetic analyses to estimate genetic and environmental correlations between circulating ICAM-1 concentration and 17 phenotypes associated with the metabolic syndrome. Our study population comprised 428 adults in 20 extended Mexican-American families from the San Antonio Family Heart Study (SAFHS). Circulating ICAM-1 concentration is heritable (h(2) = 0.56). ICAM-1 concentration showed significant positive genetic correlations (range 0.32-0.52, P < 0.05) with fasting insulin, insulin 2 h after oral glucose challenge, homeostasis model assessment of insulin resistance, BMI, waist circumference, and leptin concentration; negative genetic correlation with HDL3 cholesterol concentration; and negative environmental correlation with adiponectin concentration. Significant genetic correlations were not found between ICAM-1 and fasting or 2-h serum glucose or systolic or diastolic blood pressure. Thus, ICAM-1 expression may share common genetic modulation with traits related to obesity, insulin resistance, and HDL3 cholesterol, but not with hyperglycemia or hypertension per se.
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PMID:Intercellular adhesion molecule-1 concentration is genetically correlated with insulin resistance, obesity, and HDL concentration in Mexican Americans. 1544 2


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