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

Single administration of hydrocortisone into rabbits with experimental atherosclerosis increased the content of atherogenous classes of lipoproteins (Low Density Lipoproteins (LDL) and Very Low Density Lipoproteins (VLDL) in the animals with distinct atheromatosis. Content of the lipoproteins was decreased in animals, which had no atheromatous alterations in aorta under the effect of atherogenous diet. Within 5 hrs after the single administration of hydrocortisone in rabbits with pronounced atheromatosis of aorta relative content of cholesterol was increased in the VLDL fraction. In rabbits, resistant to development of atheromatosis, composition of VLDL was not altered. Under the effect of hydrocortisone the LDL fraction fo lipid composition was altered in the direction of relative increase in triglycerides content. In the LDL fractions subfractions were observed, which were similar to the VLDL in their cholesterol/triglycerides ratios. The data obtained suggest that in blood plasma transformation of the lipoproteins was impaired under the effect of hydrocortisone. Hydrocortisone influenced the spectrum and lipid composition of lipoproteins in blood serum independently of the degree of hypercholesterolaemia.
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PMID:[Effect of hydrocortisone on lipid composition of blood serum lipoproteins in the development of experimental atherosclerosis]. 17 72

Administration of hydrocortisone into healthy rabbits activated adenilate cyclase and phosphodiesterase in liver tissue; activity of the enzymes was normalized within 5 days after the treatment. The hormone, administered into animals with experimental cholesterol-induced atherosclerosis, caused an activation of adenilate cyclase and inhibition of phosphodiesterase; due to the phenomenon more distinct and long-term increase in cAMP concentration was observed in kidney, liver and fatty tissues. Concentration of cAMP exceeded considerably its initial content in the tissues within 5 days after the hydrocortisone administration. Hydrocortisone inhibited the adenilate cyclase system activity in adrenal cortex of experimental and control animals at early period of the experiment. In health rabbits content of cAMP was increased in adrenal cortex within 5 days after the hormone administration. As the similar effect was not found in animals with experimental atherosclerosis these data suggest that the hypophysis-adrenal cortex system under the experimental conditions studied was inhibited.
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PMID:[Effect of cortisol on adenylate cyclase and 3',5'-AMP phosphodiesterase activity and 3',5'-AMP concentration in tissues and biological fluids in experimental atherosclerosis]. 20 90

The effect of cortisol on lysosomal stability has been studied in rats fed atherogenic and normal diets. beta-Glucuronidase has been taken as a lysosomal marker enzyme. Cortisol did not significantly alter total lysosomal enzyme activity in the liver or aorta or the activity present in the hepatic nuclear fraction. However, the hormone significantly increased activity in the intact lysosome and decreased soluble activity. The ratio of soluble activity (released from the lysosomes) to activity present in the intact lysosome showed that hepatic lysosomal stability was significantly increased in rats on cortisol. Cortisol tends to restore the decreased stability observed in atheromatous rats back to that in normal rats. The rate of release of enzyme from hepatic and aortic lysosomes was reduced by cortisol in both normal and atheromatous rats. Activity of serum lysosomal enzyme was also significantly lower in rats receiving cortisol. Cortisol subsequently added in vitro after the animals had been fed a normal or an atherogenic diet caused a significant in vitro decrease in the amount of enzyme released from hepatic lysosomes. The in vitro release of enzyme from lysosomes in normal rat liver progressively fell with increasing concentration of cortisol form 10(-5)--10(-4) M. Further increase in concentration up to 5 X 10(-4) M did not significantly alter enzyme release. Since cortisol was administered as its hemisuccinate the effect of succinate on lysosomal stability was also studied. It stabilized lysosomes, but the effect was much less than with cortisol.
Atherosclerosis 1977 Jun
PMID:Cortisol and lysosomal stability in normal and atheromatous rats. 90 14

The effect of hydrocortisone on the cellular low density lipoprotein (LDL) pathway was studied in cultured human skin fibroblasts and arterial smooth muscle cells. Hydrocortisone decreased both uptake and degradation of 125I-LDL, LDL binding, measured at 4 C, was not affected by the hormone. Physiological concentrations of hydrocortisone (4 . 1 X 10(-8) mol/l) resulted in a 30% reduction of LDL uptake and degradation which could not be accounted for by an effect of the hormone on macromolecular synthesis, cell protein or cell number. To test whether the decrease in uptake and degradation of 125I-LDL was due to reduced internalization, the effect of hydrocortisone on the internalization of prebound LDL was determined and found to be decreased. Also, preincubation with unlabelled LDL in the presence of hydrocortisone resulted in less down regulation of LDL receptor activity than when no hydrocortisone was present. An effect of the hormone on bulk phase endocytosis has been excluded, since hydrocortisone did not affect either LDL degradation by receptor negative cells or endocytosis of 14C-sucrose by normal skin fibroblasts. Thus, hydrocortisone impairs LDL catabolism by decreasing the internalization of LDL normally bound to its cell surface receptor. These results may be relevant to the pathogenesis of atherosclerosis in conditions associated with reduced cellular LDL catabolism.
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PMID:Hydrocortisone decreases the internalization of low density lipoprotein in cultured human fibroblasts and arterial smooth muscle cells. 619 93

Cortisol can be implicated as contributing to a number of degenerative processes including arteriosclerosis, atherosclerosis, diabetes, and deterioration of muscle and the immune system. These effects of cortisol are amplified in diabetes due to a diminished opposition by insulin. In addition, this phenomena may not be restricted to diabetes. There is evidence that tissue sensitivity to insulin generally decreases with age, although insulin levels and metabolism may remain constant; this is not generally true for cortisol. This results in an increased cortisol activity with some pathological consequences which are most evident in vascular connective tissue and the immune system. The decrease in tissue responsiveness to insulin with respect to cortisol may reflect relative aging differences in the corresponding receptor-effector systems.
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PMID:An adventitious role of cortisol in degenerative processes due to decreased opposition by insulin: implications for aging. 626 Nov 1

Hydrocortisone-induced hyperlipemia was inhibited by physical loading in trained dogs and rabbits. Hyperlipemia simultaneously with activation of the kinin system was noted in physically untrained animals after the hormone treatment. At the same time, the patterns of lipid metabolism and of the kinin system components approached to the normal values in the trained animals. Importance of the phenomenon found for genesis of atherosclerosis is discussed.
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PMID:[Effect of physical activity on the state of the kinin system and atherogenesis]. 690 94

The role of the immunocompetent system in the development of experimental atherosclerosis was studied in experiments with 51 rabbits given hydrocortisone injections. Hydrocortisone produced atrophy of T and B systems of the lymph nodes and spleen. Under these conditions the experimental sclerosis developed little regardless high lipid blood level. This circumstance provides one more argument of the role played by the immunologic factors in the formation and development of atherosclerosis.
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PMID:[Effect of hydrocortisone on the development of experimental atherosclerosis in rabbits]. 696 95

The effect of cortisol on the synthesis of glycosaminoglycans (GAGs) was studied in cultured human aortic smooth muscle cells. Cortisol, at a level slightly exceeding the physiological concentration (10(-6) M), decreased the synthesis of hyaluronic acid (HA) by 50% but had no significant effect on the synthesis of sulphated GAGs. The ratio of HA to sulphated GAGs decreased by 47%. These effects were most marked in the fraction secreted into the culture medium. Cortisol neither affected the activity of the hyaluronic acid synthesizing enzyme complex in a cell-free system nor the molecular weight distribution of hyaluronic acid. We suggest that the atherogenity of cortisol and stress may be associated with their effect on the synthesis of HA by the smooth muscle cells of the arterial wall.
Atherosclerosis 1980 Feb
PMID:Cortisol decreases the synthesis of hyaluronic acid by human aortic smooth muscle cells in culture. 735 52

The metabolic syndrome is discussed in terms of insulin resistance linked to an increased regulation of metabolism by cortisol and fatty acids. This change in hormonal balance is associated with diabetes, android (visceral) obesity, hypertension, hypertriglyceridemia, hyperapobetalipoproteinemia and low concentrations of HDL; a cluster of risk-factors that predisposes to the development of premature atherosclerosis. It is proposed that the metabolic syndrome is accompanied by a derangement in the hypothalamic-pituitary-adrenal-axis such that the effects of cortisol are exaggerated relative to those of CRF. Excessive action of fatty acids and cortisol causes insulin resistance and increase the hepatic secretion of glucose and VLDL. Furthermore, cortisol can decrease the uptake of LDL by the liver. Cortisol in the presence of relatively high insulin concentrations can promote the deposition of energy and lead to obesity. Chronic treatment of rats with D-fenfluramine has been shown to decrease the release of cortisol and fatty acids in response to stress, and to improve insulin sensitivity. The effects of D-fenfluramine were also tested in male JCR:LA corpulent rats which are prone to develop atherosclerosis and myocardial lesions. D-fenfluramine improved insulin sensitivity, decreased the hypertriglyceridemia, and prevented the development of necrotic myocardial lesions caused by ischemia. The data presented demonstrates a link between excessive action of cortisol and fatty acids in predisposing to insulin resistance and the pathologies that are associated with the metabolic syndrome.
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PMID:Role of glucocorticoids and fatty acids in the impairment of lipid metabolism observed in the metabolic syndrome. 755 May 41

Very low density lipoproteins (VLDL) are toxic to aortic endothelial cells in vitro, and toxicity preventing activity (TxPA) inhibits this toxic effect of VLDL. Stress, an established arteriosclerosis risk factor, was examined for its effect on TxPA and on the ability of serum to protect endothelial cells from in vitro injury by VLDL. A standardized mirror tracing task with noise was administered to four healthy subjects. Blood samples were obtained at 0, 30, (stressor) 35, 50 and 80 min. Cortisol and non-esterified fatty acids increased during the stress period. TxPA significantly decreased following the stressor and had recovered by 80 min. When the ratio of non-TxPA/TxPA rose above 2, serum was no longer able to protect the cells from VLDL injury. If endothelial cells in vivo respond similarly to the endothelial cells in culture, the effect of stress on atherosclerosis may be mediated through these transient decreases in TxPA.
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PMID:Transient loss of serum protective activity following short-term stress: a possible biochemical link between stress and atherosclerosis. 772 66


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