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

Uremia is often associated with alterations in calcium metabolism and vascular smooth muscle function in hypertension and atherosclerosis. The ways in which these conditions inter-relate are not clearly understood. In order to study the possibility that circulating factors might influence smooth muscle function, experiments were performed on rat aortic strips. The serum from both uremic patients and rats enhanced the norepinephrine-induced contraction (NEIC) and net 45-calcium uptake in rat aortic strips. In a similar manner, the serum of parathyroidectomized uremic rats also increased the NEIC, whereas verapamil reduced the aortic response to levels below those of the control, in the presence of uremic serum. These findings suggest that in both chronic (patients) and early (rats) stages of uremia, there is a circulating factor, different from parathyroid hormone, that affects calcium uptake and vascular smooth muscle contraction.
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PMID:Effect of circulating factors on vascular smooth muscle contraction and its calcium uptake in uremia. 189 11

The effects of aging on atherosclerosis and osteopenia in hemodialysis patients were investigated. Eighty patients on maintenance hemodialysis were subdivided according to age into old (greater than or equal to 65 years old, N = 40) and young (less than 65 years old, N = 40). Biochemical, radiologic, and biophysical studies were performed in each patient to assess the degree of atherosclerosis and osteopenia. Compared to age-matched controls, patients in the old group exhibited a significantly higher aortic pulse wave velocity (PWV), and old female patients had a significantly lower bone mineral content/bone width (BMC/W). Elderly patients also had a significantly higher aortic PWV and higher grade of aortic calcification as assessed radiologically; in contrast, the BMC/W was lower. Concerning sex differences, elderly male patients had the highest average grade of aortic calcification, the lowest serum Pi, [Ca] x [Pi], and immunoreactive parathyroid hormone concentrations, while elderly female patients had the lowest BMC/W and highest incidence of osteopenia. These observations suggest that elderly male hemodialysis patients are more prone to develop atherosclerosis and elderly female hemodialysis patients to develop advanced osteopenia.
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PMID:A comparative study of atherosclerosis and osteopenia in elderly and young hemodialysis patients. 206 31

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

The majority of hemodialysis patients die from cardiovascular disease. However, the contribution of myocardial infarction to mortality is relatively minor, despite the fact that coronary artery disease is common in uremic patients. Hypertension seems to be the major risk factor for the development of atherosclerosis in hemodialysis patients, although abnormalities of the lipid spectrum, characterized by an increase in triglycerides and very low density lipoprotein levels and a decrease in high-density lipoprotein levels, are frequent in hemodialysis patients. The existence of left ventricular (LV) hypertrophy is a serious risk factor for morbidity and mortality in hemodialysis patients. LV hypertrophy can present as a dilated cardiomyopathy or as concentric or asymmetric septal hypertrophy. Loss of myocardial contractility by coronary artery disease or carnitine deficiency can lead to systolic LV dysfunction with a compensatory dilated cardiomyopathy. Furthermore, the presence of a hypercirculation in uremic patients, resulting from anemia, the arteriovenous fistula, or fluid overload, can also lead to a dilated cardiomyopathy. Systolic LV dysfunction occurs when the increase in LV wall thickness is inadequate for the increase in LV radius, which might be caused by increased levels of parathyroid hormone. LV diastolic dysfunction, resulting from an increase in LV mass due to the effects of hypertension or to uremic interstitial fibrosis, can both lead to pulmonary edema and hypotensive periods during hemodialysis and is a severe risk factor for mortality in hemodialysis patients. Therefore, in uremic patients, anemia should be corrected and hypertension adequately treated early in the development of renal failure. Chronic fluid overload should be prevented by adequate estimation of optimal dry weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular aspects in renal disease. 792 20

Patients with primary hyperparathyroidism have increased bone turnover, but it is less well documented how brief periods of excess parathyroid hormone (PTH) (endogenous or exogenous) affect bone metabolism. In the present double blind study, we examined the effect of either ethylenediaminetetraacetatic acid (EDTA) or placebo on serum levels of PTH and biochemical markers of bone turnover in 15 women and 39 men (aged 41 to 81 years) suffering intermittent claudication due to atherosclerosis. Disodium EDTA was administered as 20 repeated infusions of 3 grams during a period of 5-9 weeks. Serum calcium and serum phosphate decreased following treatment (p < 0.001) and remained unchanged in the placebo group. However, the differences between the groups were insignificant (ANOVA p = 0.13 and p < 0.10, respectively). PTH increased 2 1/2 fold following EDTA treatment (p < 0.001, ANOVA). The change in serum PTH was inversely correlated with the change in serum calcium (r = -0.53, p < 0.01). In the EDTA group, urinary hydroxyproline/creatinine and calcium/creatinine increased after treatment (ANOVA p < 0.001 and p < 0.05, respectively). Serum bone alkaline phosphatase decreased significantly in the EDTA group immediately after treatment (p < 0.001, ANOVA) and returned to baseline level at three months while only an insignificant decrease in serum osteocalcin was seen following treatment. We conclude that EDTA treatment increases endogenous PTH secretion considerably and leads to increased bone resorption. However, no changes in osteoblastic markers indicating increased activation of bone remodeling could be demonstrated. Our findings support that chelation therapy with EDTA is accompanied by bone loss.
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PMID:Effects of intravenous EDTA treatment on serum parathyroid hormone (1-84) and biochemical markers of bone turnover. 829 6

The preventative effects of bifemelane (4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride) on atherosclerosis in aged rats fed low-calcium diets were investigated. Male 18-month-old Wistar rats were maintained for 90 days on the following: (A) standard diet (n = 7), (B) low calcium, low magnesium, high aluminium diet (n = 8), (C) standard diet plus oral intubation with 10 mg bifemelane/kg daily (n = 6), (D) low calcium and magnesium, high aluminium diet plus oral intubation with 10 mg bifemelane/kg daily (n = 6). All groups were give these diets and water ad lib for 90 days, after which blood samples were taken from the abdominal aorta and samples of aorta were examined for atherosclerotic changes. The serum concentrations of the following were determined: calcium, magnesium, zinc, aluminium, inorganic phosphorus, cholesterol, glutamate-oxaloacetate transaminase, glutamate-pyruvate transaminase, lactate dehydrogenase, cholinesterase, creatine phosphokinase, blood urea nitrogen and N-terminal parathyroid hormone. The only significant differences between the groups in serum chemistry were reduced concentrations of cholinesterase and magnesium in groups B and D, increased aluminium in group B, and increased N-terminal parathyroid hormone in groups B and D. In groups C and D the atherosclerosis was much improved compared with that in groups A and B. It appears that bifemelane largely prevents atherosclerosis caused by calcium deposition in the arteries of rats fed low-calcium diets, due to its effect in maintaining magnesium and calcium in bones.
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PMID:Effects of bifemelane hydrochloride on atherosclerosis in aged rats fed low-calcium diets. 895 29

Cardiovascular complications account for more than 50% of death in hemodialysis patients. Strong and independent predictors of mortality or cardiovascular complications are low levels of serum albumin, high plasma C-reactive protein and lipoprotein(a), plasma proteins that are described to function as negative or positive acute phase reactants. Further prominent and known risk factors that contribute to the increased incidence of atherosclerosis in hemodialysis patients are disorders in lipoprotein metabolism and elevated plasma fibrinogen concentrations. The latter has also been described to increase following acute or chronic inflammation. The main metabolic abnormality of the lipoprotein profile is a delayed catabolism of triglyceride-rich apoB-containing lipoproteins caused by a decreased activity of lipolytic enzymes. Inhibition of lipoprotein lipase activity by cytokines or parathyroid hormone impedes conversion of very-low-density lipoprotein to low-density lipoprotein, resulting in remnant accumulation and hypertriglyceridemia. Another acute phase condition, namely, acute myocardial infarction, results in a similar pattern of dyslipidemia and coagulation disorder. In summary, the acute phase response deeply influences serum lipids and lipoproteins as well as other atherogenic acute phase proteins in hemodialysis patients. Appreciation of acute phase lipoprotein changes is essential for accurate diagnosis of dyslipidemias, proper design of future clinical studies, and correct interpretation of published data.
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PMID:Inflammation, dyslipidemia and vascular risk factors in hemodialysis patients. 935 Jun 81

Parathyroid hormone-related protein (PTHrP) appears to play crucial roles in the cardiovascular system. Over the past few years it has become apparent that there is more than one receptor recognizing parathyroid hormone or PTHrP, or both, and that PTHrP is not only a potent vasodilator of vascular smooth muscle cell tone, but is also a regulator of vascular smooth muscle cell proliferation and a secretagogue of renin and vasopressin. Investigators in several laboratories have started to query whether PTHrP intervenes in vascular diseases such as hypertension, (re)stenosis-atherosclerosis and endotoxaemia.
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PMID:Parathyroid hormone-related peptide--a smooth muscle tone and proliferation regulatory protein. 944 59

Accelerated atherosclerosis is a major risk for uremic patients undergoing long-term hemodialysis. Because hyperhomocysteinemia may influence this condition, 168 such patients were examined for a possible association between plasma total homocysteine concentration (tHcy) and conventional cardiovascular risk factors. Generalized atherosclerosis was indicated by excessive intimal-medial wall thickness (IMT) of the extracranial carotid artery as measured by B-mode ultrasonography. The results documented tHcy in these patients of 33.0+/-16.9 micromol/L, a significantly higher amount than that of healthy subjects (11.0+/-3.1 micromol/L, p<0.0001). The patients' carotid maximum IMT was 1.79+/-1.16 mm. In multiple regression analyses with forward elimination procedure, carotid maximum IMT was clearly related to age (r = 0.417, p<0.0001), systolic blood pressure (r = 0.262, p = 0.0043), smoking (r = 0.177, p = 0.0076), duration of hemodialysis (r = 0.083, p = 0.0045), and tHcy (r = 0.195, p = 0.0021). These 5 factors accounted for 36.0% of the variation in carotid maximum IMT. Factors determined as unrelated were male gender, diastolic blood pressure, body mass index, total and HDL cholesterol, triglyceride, lipoprotein(a), uric acid, calcium, inorganic phosphate, and parathyroid hormone. Therefore hyperhomocysteinemia, along with advanced age, systolic hypertension and smoking aggravates atherosclerosis in chronic uremic patients.
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PMID:Association between plasma homocysteine concentration and carotid atherosclerosis in hemodialysis patients. 1049 84


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