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)

Basal values of lecithin:cholesterol acyltransferase (LCAT) were estimated in healthy subjects, in patients with the so-called risk ischemic heart diseases (IHD)--obesity, diabetes, hypertension, and hyperlipoproteinemia II--and in patients with a IHD-infarction of the myocardium. A precise method employing a 14C-4-cholesterol-labeled common normolipidemic substrate was used. A highly significant difference in the average values of LCAT activity between healthy men and women was found. LCAT in men with 'risk' diseases decreased, while in women it remained at the level of the reference group. To assess the dependence between LCAT-dependent indicators and IHD, criteria for evaluating the deviations from reference values were proposed. The number of deviations from the reference group increased in the sequence: obesity, hypertension, diabetes, hyperlipoproteinemia, and the infarction of the myocardium.
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PMID:Lecithin:cholesterol acyltransferase as a possible diagnostic tool in ischemic heart disease. 74 40

Hyperlipidemia and lipoprotein abnormalities are often encountered in patients with nephrotic syndrome or chronic renal disease and also in those undergoing haemodialysis and with renal transplant. Even though the significance of lipid deposition in renal tissue and the role of lipoproteins in the pathogenesis of renal disease in man is unclear, experimental and clinical data indicate a possible damaging effect of a disturbed lipid metabolism on the kidney. In humans, glomerular lipid deposition is observed in genetic diseases such as Fabry's disease, lecithin:cholesterol acyltransferase activity (LCAT) deficiency and arteriohepatic dysplasia, and in diseases with acquired disturbance of lipid metabolism such as nephrotic syndrome and cholestatic liver disease. Studies on animals with lupus nephritis, aminonucleoside nephrosis, reduced renal mass, diabetes mellitus or systemic hypertension have shown that cholesterol can increase the incidence of glomerulosclerosis. As most of these studies have been performed in the rat, which has a different lipoprotein profile to that of man, these results should be carefully interpreted with regard to their relevance for humans. In vitro cell culture studies on human glomerular cells have given some preliminary insights into the cellular mechanisms of lipid induced glomerular damage. Apo E-containing lipoproteins, which are pathologically elevated in many renal diseases, are avidly taken up by human mesangial cells. These cells seem to play a central role in the initiation of glomerulosclerosis by inducing proliferation and production of excess extracellular matrix. Lipoproteins are able to stimulate DNA synthesis in these cells, and increase the synthesis of mitogens and extracellular matrix protein. The pathogenic role of oxidized lipoproteins has not yet been defined. Human mesangial cells do not seem to take up these modified lipoproteins. However, macrophages infiltrate glomeruli and may constitute the stimulus for the generation of minimally modified lipoproteins and their cellular uptake. The data from animal experiments suggest that treatment that corrects hyperlipidemia may have an ameliorative effect on renal function. Thus, there are strong indications that lipoproteins may play a critical role in mediating the development of glomerulosclerosis.
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PMID:The role of lipids in nephrosclerosis and glomerulosclerosis. 794 52

Arterial hypertension is a dominant pathogenetic factor for glomerulosclerosis. Nevertheless metabolic factors such as hyper- or dyslipoproteinemia may significantly modify and accelerate the process of glomerular scarring. Hyperlipidemia and lipoprotein abnormalities are often encountered in patients with nephrotic syndrome and chronic renal disease. Although the significance of lipid deposition in renal tissue and the role of lipoproteins in the pathogenesis of renal disease in man has not yet been clearly defined, experimental and clinical data indicate a damaging effect of disturbed lipid metabolism on the kidney. In humans glomerular lipid deposition is observed in several genetic diseases, including lecithin-cholesterol acyltransferase activity deficiency. Studies on animals with reduced renal mass, diabetes mellitus or arterial hypertension have shown that hypercholesterolemia increases the incidence of glomerulosclerosis. Especially the interaction of arterial hypertension and dyslipoproteinemia leads to a rapid and pronounced development of glomerulosclerosis. As most of these studies have been performed in the rat, which has a different lipoprotein profile than man, these results should be carefully interpreted with regard to their relevance for humans. In vitro cell culture studies on human glomerular cells have provided insight into the possible cellular mechanisms of lipid-induced glomerular damage. Apoprotein E containing lipoproteins that are pathologically elevated in many renal diseases are avidly taken up by human glomerular cells. Mesangial cells seem to play a central role in the initiation of glomerulosclerosis by proliferation and production of excess extracellular matrix. Lipoproteins are able to stimulate DNA synthesis in these cells and increase the synthesis of mitogens and matrix proteins. The pathogenetic role of modified, oxidized lipoproteins has not yet been elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arterial hypertension and hyperlipidemia as determinants of glomerulosclerosis. 830 44

The effect of a hypercholesterolemic diet (HCD) on hyperlipemia and atherogenesis was investigated using normotensive Wistar/Kyoto rats (WKY), spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP), with systolic blood pressures increasing in that order. Feeding an HCD diet containing cholesterol, cholate and suet induced hypercholesterolemia in all the strains examined as compared with a normal diet. The plasma cholesterol levels were significantly higher in WKY than in SHR and SHRSP fed the HCD diet. The HCD diet also induced hepatic fat deposition, particularly deposition of cholesteryl esters, a slight increase in aortic cholesterol deposition, and elevation of both monoenoic/saturated fatty acid ratios and linoleate/arachidonate ratios in tissue lipids. The changes induced in the three strains by the HCD diet were not positively correlated with blood pressures. The HCD diet affected hepatic acyl-CoA:cholesterol acyltransferase and plasma lecithin:cholesterol acyltransferase activities differently in WKY and SHR which, in addition to the induction of delta 9 desaturase, may partly account for the difference in the diet-induced changes in the fatty acid compositions of plasma cholesteryl esters. The results indicate that hypertension per se does not stimulate the development of hypercholesterolemia and arterial cholesterol deposition induced by an HCD diet, suggesting that other factors are involved.
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PMID:Hypertension in rats does not potentiate hypercholesterolemia and aortic cholesterol deposition induced by a hypercholesterolemic diet. 844 35

The apoA- and apoB-containing lipoprotein (LP) fractions, activity of free and linked forms of lipoprotein lipases (LPL) of liver and extrahepatic tissues, and also activity of lecithin:cholesterol acyltransferase (LCAT) were examined in the blood serum of patients with arterial hypertension, type II diabetes mellitus (DM-II), and metabolic syndrome (MS). Patients with DM-II had the most pronounced changes of all investigated LP fractions compared with healthy persons and patients of other groups examined. Decrease of LCAT activity corresponded to declining level of apoA-containing LP in DM-II and MS. Based on these data obtained we suppose, that one of peculiarities of LP metabolic disorders in the patients is a releasing of a part of lipolitic enzymes, located on the capillary endothelium, into blood flow. Heparin may have an important role in LPL redistribution, as its concentration in blood cells was declined in all the patients.
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PMID:[The lipoprotein metabolism in arterial hypertension, type II diabetes mellitus, and metabolic syndrome]. 1704 98

The aim of this study was to determine serum lecithin:cholesterol acyltransferase (LCAT) activity in parallel with HDL2 and HDL3 amounts and composition in pregnancy induced hypertension (PIH) and chronic hypertensive (CH) mothers and in their small for gestational age (SGA) newborns. LCAT activity was assayed by conversion of [3H] cholesterol to labelled cholesteryl ester. HDL2 and HDL3 were separated by ultracentrifugation. At term, cholesterol values were similar in PIH, CH and controls. However, higher levels of triglycerides were observed in PIH and CH (+20% and +21%, respectively) as compared with normotensive control mothers (NC). HDL2 and HDL3-phospholipids, HDL2-cholesterol concentrations and LCAT activity were lower in PIH and CH mothers than in NC mothers. Similar changes were also observed in SGA newborns of PHI mothers and in SGA newborns of CH mothers when compared to appropriate for gestational age newborns of control mothers (AGA-NC). In addition, SGA newborns showed low HDL2 and HDL3 apoA-I contents. Maternal hypertension and foetal intrauterine growth retardation are associated with profound abnormalities in HDL metabolism, consistent with an atherogenic risk. SGA lipoprotein profiles appear to implicate later metabolic diseases.
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PMID:Serum lecithin: cholesterol acyltransferase activity, HDL2 and HDL3 composition in hypertensive mothers and their small for gestational age newborns. 1760 41

Familial lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare metabolic disease with lipid deposition in several organs. The authors report a man with hypertension and proteinuria. Renal biopsy revealed glomerular changes, including peculiar thrombus-like deposits, consistent with LCAT deficiency. He was found to be compound heterozygous for two mutations of the LCAT gene. He received a kidney graft from his father. The authors also describe LCAT deficiency-related lesions in the explanted native kidneys and in biopsies at 2 days, 6 weeks, and 1 year after transplantation. The morphology of this disease is characteristic, and the diagnosis should be suspected from the ultrastructural findings.
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PMID:Lecithin: Cholesterol Acyltransferase (LCAT) Deficiency: renal lesions with early graft recurrence. 2132 22

Familial lecithin-cholesterol acyltransferase (LCAT) deficiency is a rare autosomal recessive (AR) disease caused by mutation in the LCAT gene. LCAT enzyme esterifies cholesterol molecules in high-density lipoprotein(HDL) and low density-lipoprotein (LDL) particles. This enzyme deficiency is characterised by progressive corneal opacification, glomerulopathy, mild - moderate haemolytic anaemia and very low plasma levels of HDL. We here report a 34 year-old lady who presented with hypertension, nephrotic proteinuria, renal failure, corneal ring opacities, anemia and dyslipidemia. The diagnosis of familial LCAT deficiency was confirmed by clinical examination, characteristic dyslipidemia, undetectable LCAT levels in plasma and positive family history.
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PMID:Familial Lecithin Cholesterol Acyl Transferase Deficiency with Chronic Kidney Disease. 2776 13