Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concern about a possible association between oral contraceptives (OCs) and cardiovascular problems has led to investigation of the effects of OC use on plasma lipids and lipoproteins. The lipoprotein metabolic system involves chylomicrons derived from dietary fat, very-low-density lipoproteins (VLDL) derived primarily from the liver, and high-density lipoproteins (HDL). VLDLs form remnantlike particles termed intermediatedensity lipoproteins (IDLs), which ultimately are converted to low-density lipoproteins (LDLs). Understanding of how these particles relate to the atherogenic process is incomplete, although the spectrum of VLDL-LDL particles is involved in atherosclerosis. Whereas the LDLs and IDLs can deliver cholesterol to the artery wall, the HDLs seem to be involved in bidirectional cholesterol transport and are capable of accepting cholesterol from tissues and other lipoprotein classes. This property has caused HDL to become known as an antiatherogenic lipoprotein. Estrogen appears to increase VLDL production rates as well as the clearance of remants and LDL, although genetic factors may be involved. Estrogen's effect on HDL seems to be a more uniform increase in production. In contrast, synthetic progestational steroids appear to reduce HDL, in part due to the increased metabolism of HDL lipids mediated by hepatic lipase activity. They appear to interact with estrogen to raise LDL and VLDL levels. Epidemiologic studies suggest that low- and high-density cholesterol provide the best clinical indices of cardiovascular risk. When the HDL level is low, coronary risk amplifies; when the HDL level is high, the LDL effect on coronary risk compresses. There is as yet no precise information on the extent to which changes in lipoproteins, especially HDL, affect the development or progression of coronary artery disease.
 ...
PMID:Effects of oral contraceptives on lipid metabolism. 372 87

Estrogen replacement therapy (ERT) is the most effective treatment for vasomotor hot flushes and urethrovaginal atrophy in postmenopausal women. Evidence also suggests that ERT delays osteoporosis and may even reduce the risk of atherosclerosis. Despite continuing controversy, the risks of ERT are now considered minimal. With individualized therapy and appropriate monitoring, ERT with progestin supplements appears to be safe and effective for the great majority of postmenopausal women.
 ...
PMID:Is estrogen replacement therapy necessary? 407 11

This study examines the effects of diethylstilbestrol administration on thrombocyte aggregation and thromboxane B2 synthesis. Diethylstilbestrol (10 mg/kg in sesame oil) was injected intramuscularly each week for 2 weeks in female white Carneau pigeons who were susceptible to atherosclerosis. Blood samples were drawn from the heart, titrated and centrifuged. Washed platelets were isolated and suspended for use in experiments involving incubation with C14-arachidonic acid. Gas-liquid chromatography was used to determine fatty acid composition of platelet phospholipids. The estrogen-treated thrombocytes exhibited more aggregatory response to arachidonic acid than those of control birds. To determine whether synthesis of proaggregatory thromboxane A2 (measured as thromboxane B2) by platelets is affected, conversion of C14-arachidonic acid into various prostaglandins by platelets was measured. Synthesis of thromboxane B2 in DES-treated thrombocytes was significantly higher (p0.05) than in normal thrombocytes. No significant difference was found in the formation of other prostaglandins. Total phospholipid level (mcg/mg protein) was higher in DES-treated platelets (18.2 +or- 3.5 in control thrombocytes vs. 26.7 +or- 3.1 in DES-treated thrombocytes). The study shows that diethylstilbestrol stimulates thrombocyte aggregation, confirming the report of increased platelet aggregation in women on oral contraceptives.
 ...
PMID:Enhancement of thrombocyte aggregation and thromboxane B2 synthesis by diethylstilbestrol. 722 May 91

Estrogen is known to retard the development of atherosclerosis and to work in the brain, but the mechanism of hormonal action is completely unknown. We investigated the effect of estrogen on the activity of neuronal constitutive nitric oxide synthase (NNOS). A low concentration of estrogen (10(-10)(-7) M) enhanced the activity of homogenates of the cytosol fraction of rabbit cerebellums and also that of partially purified NNOS, and high dose (10(-6)(-5) M) attenuated them. The study using estrogen receptor antagonists, tamoxifen, clomiphene, and ICI182780 suggested that estrogen receptor did not relate significantly to those effects of 17 beta-estradiol. 17 alpha-estradiol or progesterone did not change significantly it in low doses, although moderately inhibited it in high doses. Estrogen enhanced the fluorescence of dansyl-calmodulin in low doses and attenuated it in high doses, suggesting that estrogen affects Ca(2+)-calmodulin directly. This study demonstrated that estrogen has a biphasic effect on the activity of NNOS through a Ca(2+)-calmodulin.
 ...
PMID:Biphasic effect of estrogen on neuronal constitutive nitric oxide synthase via Ca(2+)-calmodulin dependent mechanism. 752 39

The prevalence of coronary artery disease is lower in women than in men. Ovarian estrogen is believed to decrease the risk of coronary heart disease. Today, there is an increasing demand for estrogen replacement not only for amelioration of menopausal subjective symptoms but also for the prophylactic action of estrogen against osteoporosis in postmenopausal women. Is generally agreed that estrogen replacement therapy reduces cardiovascular morbidity and mortality in postmenopausal women. Estrogen replacement therapy may protect against coronary heart disease by altering plasma lipoprotein concentrations, by increasing HDL cholesterol and decreasing LDL cholesterol, and thereby inhibiting progression of coronary artery atherosclerosis. Oral contraceptive can induce deterioration in glucose tolerance that has consistently been associated with insulin excess and insulin resistance. This situation can increase the coronary heart disease risk. New findings suggest that there may be independent cardioprotective effects of estrogen, such a direct inhibitory influence on thrombosis, vasospasm or atherogenesis, inhibiting atherosclerotic plaque formation in arterial walls.
 ...
PMID:[Sex hormones, glycolipid metabolism, and atherogenesis]. 756 60

Low-dose estrogen replacement therapy should be recommended to post-menopausal women, especially if they suffer from circulatory disorders, because it significantly reduces cardiovascular risk. Low-dose estrogens favourably affects lipid profile, without causing a significant increase of thrombotic risk: atherosclerosis is therefore prevented. Estrogen can augment coronary flow by the relaxation of vascular smooth-muscular cells. Finally, estrogen can improve left ventricle systolic and diastolic function, delaying the physiological aging process.
 ...
PMID:[Estrogens, left ventricular function and coronary circulation: what are the possibilities of therapeutic use?]. 764 87

Estrogen use is associated with protection from cardiovascular disease in postmenopausal women. This benefit appears to be magnified among women with pre-existing heart disease. The possible bias of intrinsically better health in women using estrogen has not been ruled out in observational studies. Therefore, two double-blind randomized clinical trials are underway in postmenopausal women. One in women with coronary disease is known as HERS (Heart Estrogen-progestin Replacement Study) and another in predominantly healthy women is the WHI (Women's Health Initiative). Several mechanisms of estrogen mediated protection from cardiovascular disease have been identified including increased HDL, lower LDL, lower VLDL-cholesterol/triglyceride ratio, increased clearance of intermediate density lipoprotein (IDL) and LDL via an upregulated LDL receptor, diminished penetration and degradation of LDL in the arterial wall, an inhibition of LDL oxidation by various estrogens and a reversal of inappropriate acetylcholine (EDRF)-mediated vasoconstriction in arteriosclerotic vessels. The predominating mechanism is not known, but estrogen replacement therapy is both likely to be beneficial to female health, pending randomized trials, as well as a tool to understand mechanisms of prevention of coronary artery disease.
Atherosclerosis 1994 Oct
PMID:Effects of estrogens on lipoprotein metabolism and cardiovascular disease in women. 785 90

High concentrations of lipoprotein(a) [Lp(a)], an independent risk factor for atherosclerosis, cannot be managed by the usual lipid-lowering agents. It has been suggested that Lp(a) levels are related to female sex hormones. Estrogen replacement therapy makes the lipid profiles favorable for delaying atherosclerosis in postmenopausal women. The effects of the combination therapy of estrogen and progesterone on lipids are controversial. This study was designed to evaluate the effect of female sex hormones on the concentration of Lp(a) and to clarify the influence of progesterone on the effect of estrogen in postmenopausal women. Postmenopausal women (n = 184) were divided into four groups: control; 0.625 mg conjugated equine estrogen (CEE) plus 10 mg medroxyprogesterone acetate (MPA); 0.625 mg CEE plus 5 mg MPA; and 0.625 mg CEE only. Medication for 2 months lowered the concentrations of Lp(a) by 20% in all treated groups. The decrease was more pronounced in subjects with a relatively higher basal Lp(a) concentration. Estrogen replacement therapy raised the concentration of high-density lipoprotein cholesterol and decreased low-density lipoprotein cholesterol without changing total cholesterol. The combination therapy of estrogen and progesterone abolished the effect of estrogen on high-density lipoprotein cholesterol. Hormone replacement therapy lowered Lp(a) levels in postmenopausal women. The effect was prominent in subjects with high basal Lp(a) levels. This decrease may be one of the mechanisms of the cardioprotective effects of estrogen. The cardioprotective effect of estrogen cannot be applied to the combination therapy due to the adverse effect of progesterone on high-density lipoprotein cholesterol.
 ...
PMID:Effects of hormone replacement therapy on lipoprotein(a) and lipids in postmenopausal women. 830 20

The JCR:LA-cp rat exhibits an obese, insulin resistant, hyperlipidemic syndrome. Obese male rats, only, develop atherosclerosis and ischemic myocardial lesions. The obese males have a greater hyperinsulinemia, but the obese females have a much greater hypertriglyceridemia due to hypersecretion of very low density lipoprotein (VLDL). Obese rats of both sexes were surgically castrated at 6 weeks of age to study the influence of testosterone and estrogen secretion on the sexual dimorphism of metabolism and disease in this strain. Castration had no effect on body weight or food consumption up to 16 weeks of age. Castrated male rats had significantly improved glucose tolerance, but a doubled serum triglyceride concentration. Castrated female rats showed approximately halved triglyceride levels. The distribution of the triglyceride molecular species was altered in the castrated male rats to resemble that of the females in which there was no change with castration. The effects suggest that testosterone may inhibit hepatic triglyceride secretion and promotes insulin insensitivity. Estrogen appears to exacerbate hepatic hypersecretion of VLDL. Castration had no effect on myocardial lesion frequency in 9-month-old rats of either sex. This implies that estrogen does not exert a direct protective effect against cardiovascular disease in this animal model.
Atherosclerosis 1993 Apr
PMID:Effect of castration on hyperlipidemic, insulin resistant JCR:LA-corpulent rats. 831 56

It has been demonstrated that high cholesterol levels are correlated with development of atherosclerosis, while high levels of high density lipoprotein (HDL) are associated with reduced cardiovascular mortality. Some endocrine disorders accelerate atherosclerosis in association with hypercholesterolemia, hypertension, low level of HDL and hypertriglyceridemia. In patients with acromegaly, hypertriglyceridemia is sometimes accompanied with and aggravated by the presence of impaired glucose tolerance. In patients with hypothyroidism, coronary atherosclerosis may develop in association with hypertension, hypercholesterolemia and moderate elevation of triglyceride which is often accumulation of intermediate lipoprotein. Cushing syndrome may accelerate atherosclerosis by the fact that corticosteroid may induce or exacerbate several known coronary risk factors including hypertension, hypercholesterolemia and impaired glucose tolerance. Estrogen has beneficial effects on the cardiovascular system for postmenopausal women by affecting lipid metabolism, decrease of LDL and increase of HDL.
 ...
PMID:[Atherosclerosis and endocrine disorders]. 841 91


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>