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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the light potential preventive pharmacotherapy of experimental atherosclerosis, attention has been focused on the effect of some substances tested in models that may represent human atherosclerosis. Calcium antagonists of various chemical groups administered simultaneously prevent the accumulation of calcium in cells under conditions of experimental calcinosis and atherosclerosis, as e.g. in spontaneously hypertensive rats, in rabbits on cholesterol diet, at administration of high doses of vitamin D, and on using the cuff technique. The results indicate that substances involved in the metabolism of calcium affect basic pathogenic processes of calcinosis and atherosclerosis.
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PMID:[Present methods of inducing calcinosis and atherosclerosis and perspectives of pharmacologic prevention]. 268 8

Recent studies from several laboratories have shown perturbations of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] metabolism in hypertension. While these perturbations may exert their effect on blood pressure via their actions on calcium metabolism, it is possible that this vitamin D metabolite may have direct effects on vascular smooth muscle cell (VSMC) physiology. To examine this, we studied the effect of 1,25(OH)2D3 on VSMC growth and found that this substance suppressed VSMC [3H]thymidine uptake; furthermore, this vitamin D metabolite also suppressed the stimulatory effect of epidermal growth factor (EGF) on VSMC proliferation. The concomitant presence of this substance appeared to be required for its action on VSMC growth since cells pretreated with the vitamin D metabolite for up to 72 hours and then washed of the substance grew normally and responded to EGF. Studies were also done to determine if 1,25(OH)2D3 had any effect on the function of EGF receptors on VSMC. Experiments using Iodine-125-labeled EGF showed no differences in the binding of this ligand to VSMC, either untreated or treated with 1,25(OH)2D3, which indicates the effect of the vitamin D metabolite on VSMC growth (when exposed to EGF) was not mediated by an alteration of EGF receptor function. The results of these studies have implications for the pathogenesis of vascular diseases such as hypertension and atherosclerosis.
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PMID:1,25-Dihydroxyvitamin D3 and rat vascular smooth muscle cell growth. 278 49

The inhibitory effect of elastase on experimental atherosclerosis has been reported in numerous studies. In our investigation, performed in the rat, a pancreatic extract provided with elastolytic activity has been shown to possess an anti-aggregative effect in vitro and ex vivo and anti-thrombotic properties. In addition, the elastase was capable of inhibiting endothelial exfoliation induced by the desquamatory agent sodium citrate. This agent was tested for its microhaemorrhoeological activity in acute and subacute experiments. In both these conditions, elastase was able to increase the flexibility of red blood cells and their resistance to lysis provoked by hypotonic solutions. In animals fed on an atherogenic diet, this substance limited the lipoprotein accumulation in the aorta wall. Moreover, it reduced the enhanced calcium content, induced by vitamin D administration, in the tissue of arteries. These data indicate that elastase can counteract some pathobiological aspects that characterize atherosclerotic events.
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PMID:Biological properties of pancreatic elastase in relation to atherosclerotic disease. 325 Sep 37

Drugs influencing calcium metabolism in animals fed high-fat diets may modify the progression of atherosclerosis. Agents that enhance calcium transport (catecholamines, vitamin D, parathyroid hormone) may accelerate atherogenesis. Conversely, agents with calcium chelating (diphosphonic acid and thiophene carboxylic acid derivatives), calcium channel blocking (dihydropyridine derivatives, verapamil and its derivatives, diltiazem), and anti-adrenergic (beta-blockers) properties have been demonstrated to suppress atherogenesis in rabbits and monkeys. Possible mechanisms of action include lowering of arterial pressure, minor changes in circulating lipoproteins, altered receptor-dependent lipoprotein uptake and lipoprotein metabolism, inhibition of cell migration and cell proliferation, and non-specific protection of injured cells in atheromatous lesions.
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PMID:Anti-atherosclerotic effects of calcium antagonists: a brief review. 332 99

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

Effects of supplemental dietary calcium and vitamin D on lipid distribution and aortic mineralization were examined in young goats. Twenty-four goats, 2-4 wk of age, were allotted one of four dietary treatments for a 20-wk period and fed a basal milk diet (Basal), a calcium-supplemented diet (Basal + Ca), a cholecalciferol-enriched diet (Basal + D3) or a diet with both calcium and cholecalciferol (Basal + Ca + D3). Goats in the Basal + Ca group had plasma cholesterol concentrations that were 16.6% of those of the Basal group. Percentage absorption and fecal excretion of total lipids were unaffected by dietary treatment. Generally, total lipid and cholesterol concentrations were unaltered in liver, other viscera and carcass tissues. Dietary cholecalciferol increased concentrations of cholesterol and total lipid in aortas, whereas dietary calcium decreased total lipids in aortas. Concentrations of calcium, magnesium and total ash were increased in aortas by dietary treatment, with a marked increase observed in the Basal + Ca + D3 group. Sudan IV and gross calcium staining in aortas revealed both lipid and mineral deposition that confirmed composition data. A high intake of vitamin D accompanied by excessive intake of calcium seems to accelerate the development of atherosclerosis. Supplemental calcium with normal amounts of vitamin D, however, is hypocholesterolemic and seems protective against the atherogenic process.
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PMID:Dietary calcium and vitamin D: risk factors in the development of atherosclerosis in young goats. 396 86

The Department of Steroid Biochemistry headed by Professor Vendt Volodymir Petrovich, Doctor of Biological Sciences (1906-1993) was created on the basis of the Department of Photobiochemistry in 1976. At that time the Department was headed by Kokunin Vasyl Andriyovich, Candidate of biological sciences, till 1990. Professor Yu.D.Kholodovais, Doctor of biological sciences, is the head of the department today. Study of action mechanism of low-molecular-weight biologically active substances of steroid nature (cholesterol, cholecalciferol, ecdysterone) under normal and pathological conditions (atherosclerosis, rickets) as well as the development of scientific grounds of production of new drugs used both in medicine and agriculture are the basic purposes of the Department. The department is engaged in: 1) the study of biosynthetic processes of de novo cholesterol and its precursors in different tissues and cells of the organism; 2) the elucidation of the role of sterols as the components of membrane structure in different cells as well as the study of cholesterol absorption processes in the intestine and the search of a hypocholesterolemic agents; 3) the study of localization and biological properties of vitamin D-dependent proteins in order to elucidate their role in intestinal calcium transport; 4) the investigation of different classes of blood plasma composition of intestine and liver lipoproteins (LP), their structural, functional properties and frequency of occurrence; 5) the search of highly effective biostimulators of steroid nature, the elucidation of their action mechanisms and elaboration of new preparations on their basis for medicine and agriculture. Sterols are components of lipids with cyclopentanoperhydrofenantren molecular structure. Cholesterol is the basic animal and human organism sterol. A new complicated, multi-step method of cholesterol biosynthesis and participation of a number of enzymes and cofactors in it have been studied (V. Vendt, R. Morozova, I. Nikolenko, Visnyk AN URSR, 1978). Cholesterol is the major component of cell membrane structures which determines their structure and permeability. The interest to study a new method of cholesterol biosynthesis regulation arises from the reason that cholesterol pools in membranes participate in such diseases as rachitis, atherosclerosis, arterial coronal disease, different forms of cholecystitis, etc. It is established that the nature, rate and intensity of de novo cholesterol biosynthesis depend on types of cells, tissues and organs, taking into account the functional state of final compounds in these biosystems under normal conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Department of sterol biochemistry]. 757 Oct 72

Glucocorticoids are highly valuable medication available to a physician, yet, their serious side effects have severely limited their use. Thus, the major purpose of our review is to provide a practical approach to increasing efficacy and minimizing side effects, that is increasing the benefit/risk ratio, of glucocorticoid therapy. The most effective way of avoiding their side effects, including infection, osteoporosis, atherosclerosis, is simply to avoid the overuse of glucocorticoids and to restrict their use to the truly indicated disease. Side effects can be reduced in part by the development of drug delivery systems, such as topical administration and targeting therapy. Combinations of calcium, vitamin D and sometimes thiazide or calcitonin, as compensatory therapy, have shown some favorable results for the prevention of osteoporosis. Although glucocorticoid therapy causes an increase of high-density lipoprotein and a decrease of lipoprotein (a) in serum, both are possibly preventive for atherosclerosis, hypertension and diabetes mellitus which are risk factors of atherosclerosis should be controlled. Future trends to remove their side effects will be obtained by more specific therapy based upon their pathogenesis.
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PMID:[Minimizing side effects of glucocorticoid therapy]. 816 80

Our views on paediatric nutrition have considerably changed during the last 20 years. Some hereditary metabolic diseases testify to the remarkable efficacy of a specific preventive dietetics avoiding the development of mental retardation. Although certain deficiencies (in iron, fluorine, folates, vitamin D) are persisting in France, the major problems concern the prevention in childhood of allergy, obesity, atherosclerosis, high blood pressure, osteoporosis and even certain cancers, all diseases which play a crucial role in the morbidity and mortality of adults. Numerous uncertainties still exist, but in the present state of our knowledge we can already develop some recommendations which should replace the much abusive publicity that prevails in the information given to the public.
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PMID:[Towards preventive dietetics in children]. 850 35

The human apoSAA proteins comprise both acute phase (apoSAA1, apoSAA2) and constitutive (apoSAA4) isoforms; all are expressed in human atherosclerotic lesions as well as in liver. Recombinant acute phase apoSAA binds cholesterol with an affinity of approximately 170 nM and enhances cholesterol uptake by HepG2 cells (J. Lipid Res. 1995. 36:37-46). In the present study, we sought to define the region of acute phase apoSAA involved in cholesterol binding and to investigate the ability of constitutive apoSAA4 to bind cholesterol. Binding of [3H]cholesterol to apoSAAp was inhibited by unlabeled cholesterol (1-100 nM), but not significantly by vitamin D and estradiol. Direct binding of acute phase, but not constitutive, apoSAA to the surfaces of polystyrene microtiter wells was strongly diminished in the presence of cholesterol. The ability of apoSAAp to bind cholesterol was inhibited by antibodies to human apoSAA1 and to peptide 1-18 of apoSAA1. There was only slight inhibition of cholesterol binding by antibodies to peptide 40-63, and no inhibition by antibodies to peptides spanning regions containing amino acid residues 14-44 and 59-104. [3H]cholesterol uptake by neonatal rabbit aortic smooth muscle and HepG2 cells was enhanced by a synthetic peptide corresponding to amino acids 1-18 of hSAA1, but not by peptides corresponding to amino acids 1-18 of hSAA4. [3H]cholesterol uptake by HepG2 cells was slightly increased by a peptide corresponding to amino acids 40-63 of hSAA1. These findings suggest that apoSAA modulates the local flux of cholesterol between cells and lipoproteins during inflammation and atherosclerosis.
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PMID:Amino terminal region of acute phase, but not constitutive, serum amyloid A (apoSAA) specifically binds and transports cholesterol into aortic smooth muscle and HepG2 cells. 890 88


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