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)

Recently, food intake in Japan has been characterized by an increase in fat intake, especially animal-fat intake and the maintenance of excess salt (sodium chloride) intake. It is generally accepted that the increase in fat intake is closely related to atherosclerosis, and excess salt intake is a high risk factor for the development of hypertension and cerebrovascular lesions. So far, in almost all reports, the increase in fat intake and excess salt intake have been studied independently, and there have been few reports on the combined effects of these two factors. Taking the above things into consideration, it would seem to be very interesting to investigate the effect of excess salt intake on lipid metabolism. In this paper, we studied the effects of excess salt intake on lipoprotein and apolipoprotein metabolisms, using stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Kyo: Wistar rats (WKY) as model animals. The results obtained were as follows: A significant increase in the concentration of serum total cholesterol (TC) was observed in SHRSP and WKY, when the rats were given a regular diet (CE-2, Clea Japan Inc.) and 1% sodium chloride solution (1% NaCl) as drinking water for 4 weeks. This was accompanied by a tendency toward increases in the concentrations of serum apolipoproteins in both strains. These results suggest that excess salt intake could accelerate the production of serum total lipoproteins in SHRSP and WKY, when the rats are fed a regular diet. Next, 1% NaCl and a high-fat and high-cholesterol diet (HFC diet) were simultaneously given to SHRSP and WKY for 6 weeks. The effects of simultaneous administration on lipoprotein and apolipoprotein metabolisms were compared with those of HFC feeding. One percent NaCl did not markedly affect hypercholesterolemia in WKY, while it induced more marked hypercholesterolemia in SHRSP that was associated with extreme elevations of serum TC and the atherogenic index (A.I.). This deleterious effect of 1% NaCl in SHRSP was due to drastic elevations of cholesterol contents in the very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) fractions. This was also associated with marked increases in apo B contents in the VLDL, IDL and LDL fractions and significant increases in apo E contents in the VLDL and IDL fractions. These results indicate that 1% NaCl induced much larger increases in serum atherogenic beta-lipoproteins in SHRSP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-fat and high-cholesterol diet--effects of salt intake on serum lipoprotein and apolipoprotein metabolism]. 263 85

Changes in serum lipids, apolipoproteins, and lipoproteins including high-density lipoprotein (HDL) subfractions following administration of captopril in patients with hypertension were studied. Captopril (25 mg twice daily) was administered over a 12-week period to 17 patients with mild to moderate essential hypertension. Captopril was observed to significantly reduce both systolic and diastolic blood pressure, as well as to increase HDL2- cholesterol (HDL2-C) and to decrease HDL3-cholesterol (HDL3-C); however, no significant changes in total HDL-C were recognized. Total cholesterol, low-density lipoprotein cholesterol, triglyceride, apolipoprotein (apo) A-I, apo A-II, apo B, apo C-II, apo C-III, and apo E did not change significantly. It is suggested that captopril monotherapy produces a favorable effect on HDL subfractions.
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PMID:Effect of captopril on high-density lipoprotein subfractions in patients with mild to moderate essential hypertension. 265 2

A systematic study of 100 elderly patients in a hospital geriatric unit was undertaken to analyse the relationship between clinical cardiovascular events (angina, myocardial infarction, hypertension, cerebrovascular accidents, temporo-spatial disorientation, invalidity, incontinence) and plasma lipids (total cholesterol, HDL and LDL fractions, triglycerides, apolipoprotein A and B and total cholesterol/HDL and apolipoprotein B/A ratios). The average triglyceride and apolipoprotein A concentrations were related to the patient's validity: The triglycerides were significantly higher in the group of invalid patients (+22%), p = 0.05. The apolipoprotein A levels were significantly lower in the invalid group (-12%), p = 0.05.
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PMID:[Assays of apolipoproteins A and B as atherogenicity factors in aged patients at hospitals]. 266 Jun 51

The effects of bunazosin and propranolol administration on hypertension and serum levels of lipids, lipoproteins and apolipoproteins were studied in a controlled, randomized multicenter study. After a 4-week washout period, 48 patients with mild to moderate essential hypertension were randomly assigned to either the bunazosin or the propranolol group. Twenty-four were treated with bunazosin (1 to 3 mg t.i.d.) and 24 with propranolol (10 to 40 mg t.i.d.) for 12 weeks. Systolic and diastolic blood pressures decreased significantly in both groups. After 12 weeks of bunazosin treatment, significantly lowered apolipoprotein (apo) B and apo B/apo A-I ratio (p less than 0.05, in both cases) were observed, in contrast to no changes in the propranolol group. Although the changes were not significant, bunazosin tended to decrease the ratio of total cholesterol minus HDL cholesterol to HDL cholesterol. There were no significant changes in total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, apo A-I, apo A-II, apo C-II, apo C-III and apo E for either bunazosin or propranolol. The difference between the two drugs was significant for the apo B/apo A-I ratio (p less than 0.05). Bunazosin monotherapy was shown to be as effective in reducing blood pressure as propranolol. In addition, its favorable effects on lipoprotein metabolism seem to offer an additional advantage in mitigating coronary risk.
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PMID:Comparative effects of bunazosin and propranolol on serum lipids and apolipoproteins in patients with essential hypertension. 267 72

Serum lipids, lipoproteins, and major apolipoproteins and their association with previous myocardial infarction were studied in patients with non-insulin-dependent diabetes mellitus (NIDDM) and nondiabetic subjects in East and West Finland in 1982-1984. NIDDM patients had higher age-adjusted serum triglyceride and apolipoprotein B levels and a higher apolipoprotein B/apolipoprotein A-I ratio, lower serum high density lipoprotein (HDL) cholesterol and apolipoprotein A-1 levels, and a lower HDL cholesterol/apolipoprotein A-1 ratio than nondiabetic subjects. With a few exceptions, these differences persisted after adjustment for body mass index, alcohol intake, physical activity, smoking, and hypertension, which suggests that the atherogenic serum lipoprotein pattern in NIDDM is an inherent feature of the disease. In general, the association of serum lipids, lipoproteins, and apolipoproteins with myocardial infarction was similar in nondiabetic subjects and NIDDM patients, although it was somewhat stronger in the diabetic subjects. A low serum HDL cholesterol/apolipoprotein A-1 ratio, which was closely linked to high serum triglyceride level, seemed to be more consistently related to myocardial infarction in NIDDM patients than in nondiabetic subjects. Serum lipids, lipoproteins, and apolipoproteins, either separately or in various combinations, could only to a small extent explain the higher prevalence of myocardial infarction in diabetic subjects compared with nondiabetic subjects when tested in multivariate analysis with other cardiovascular risk factors as background variables. The association between serum lipoproteins and myocardial infarction was largely similar in East and West Finland, two areas that differ markedly with respect to the occurrence of coronary heart disease.
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PMID:Serum lipids, lipoproteins, and apolipoproteins and the excessive occurrence of coronary heart disease in non-insulin-dependent diabetic patients. 277 12

Traditional twin studies have resulted in higher concordance rates for premature coronary heart disease (CHD) in MZ than in DZ twin pairs. This is in agreement with strong evidence from several other studies, that genetic factors are of importance in the etiology of early onset CHD. Also, in a study of 291 Norwegian twin pairs the concordance rate for hypertension wa 0.36 in MZ and 0.08 in DZ pairs. Relationship between diseases and traditional gene markers have been extensively studied and several associations have been uncovered for CHD. Our group has developed a method to examine a possible permissive or restrictive effect of single genes on the degree of variation that environmental and/or life style factors can cause in a given parameter. This method for studying gene-environment interaction is based on the fact that MZ twins are identical with respect to genes, so that any difference between the two members of an MZ pair must necessarily be caused by environmental or life style factors. The possibility that a given gene influences the degree of variability in a parameter such as cholesterol is examined by comparing the within-pair difference in cholesterol level between MZ pairs possessing, and MZ pairs lacking the gene in question, and results of such studies will be presented. New possibilities to study restriction fragment length polymorphisms (RFLPs) at apolipoprotein loci have added a new dimension to research on genetics of CHD and hyperlipidemias. Association between apolipoprotein B, cholesterol and fasting triglyceride levels on one hand and DNA variation at the apolipoprotein B locus on the other has been found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Twin studies of coronary heart disease and its risk factors. 297 Jan 98

Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors--dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia--likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 +/- 10 vs 172 +/- 7 mg/dl [standard error of the mean], p less than 0.001), LDL cholesterol (140 +/- 9 vs 101 +/- 6 mg/dl, p less than 0.001), and LDL apolipoprotein-B (108 +/- 16 vs 80 +/- 16 mg/dl, p less than 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin. 305 23

Twenty-one patients with mild or moderate hypertension were randomised to receive either Atenolol 100 mg (N = 10) or Pindolol 15 mg (N = 11) in a once daily dosage over a two month period. The effects of these two betablockers on the blood pressure and plasma lipid profile were studied. Special attention was paid to the methodology: obese patients (30% over theoretical weight derived from the Lorenz formula) and those with pre-treatment triglyceride levels higher than 1.82 mmol/l were excluded because of the well documented biological instability of such patients. The selected patients were given placebo for two weeks. At the end of the placebo period those subjects whose body weight, total cholesterol, apolipoproteins or triglycerides had varied by more than 10%, 15% and 30% respectively, were also excluded from the study. At the end of the 60 days active treatment period, a comparable fall in the blood pressure was observed in both groups and there was no significant difference in the biological parameters as compared with pre-treatment values. In addition, the cardiovascular risk, evaluated by the B/A1 apolipoprotein ratio, increased in only one patient in the group receiving Atenolol and one patient receiving Pindolol.
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PMID:[Comparative effects of pindolol and atenolol on blood pressure and lipids in mild to moderate arterial hypertension]. 307 94

The purpose of this study was to elucidate the relationship between two genetic factors associated with raised blood cholesterol, i.e. familial hypercholesterolemia (FH) and apolipoprotein (apo) E4. A group of 50 unrelated heterozygous FH patients aged 33-71 years were studied together with 129 normolipidemic subjects. A significantly higher frequency of apo E4 phenotypes was found in FH patients (30.0%) than in normolipidemic subjects (15.5%). FH patients were divided into two groups with and without apo E4. Plasma total cholesterol (Chol) and triglyceride (TG) levels were significantly higher, and plasma low density lipoprotein-cholesterol (LDL-Chol) level tended to be higher in FH patients with apo E4 than in those without apo E4. In addition, the prevalence of ischemic heart disease (IHD) was significantly higher in FH patients with apo E4 (73.3%) than in those without apo E4 (31.4%). No significant difference was noted in age and in the prevalence of obesity, diabetes, hypertension and smoking between the FH groups with and without apo E4. These results suggest that apo E4 is associated with higher levels of total Chol and TG and, at least in part, contributes to the predisposition to IHD in FH.
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PMID:Familial hypercholesterolemia and apolipoprotein E4. 321 64

Intimal lipid concentrations were determined in aortic biopsies obtained during coronary by-pass surgery. In addition serum lipoprotein and apolipoprotein levels were quantitated and their relationships to aortic intimal lipid concentrations were analysed. The possibility to use aortic intimal lipid and serum lipoprotein or apolipoprotein concentrations to predict clinical prognosis following the coronary by-pass operation was also evaluated. Intimal cholesterol, cholesterol ester, phosphatidylcholine and sphingomyelin were intercorrelated, whereas none of these lipid fractions correlated to aortic intimal triglyceride levels. Patients with hypertension had higher aortic intimal cholesterol ester levels than normotensive patients. There was a positive correlation between the number of stenosed coronary arteries and serum apo B or triglyceride levels. In addition there was a negative correlation between the number of stenosed arteries and HDL-cholesterol. Prognosis after the operation was inversely correlated to serum apo A-I levels. Our data do not, however, support the notion that aortic intimal lipid levels can be used to evaluate prognosis after coronary by-pass surgery.
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PMID:Aortic intimal lipid content and serum lipoproteins in patients undergoing coronary by-pass surgery as related to clinical prognosis. 326 59


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