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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

Computed tomographic (CT) findings of cerebral and cerebellar calcification are described in three American adults with raised serum lead levels and known exposure to lead for 30 or more years. Calcification patterns were punctiform, curvilinear, speck-like, and diffuse and were found in the subcortical area, basal ganglia, vermis, and cerebellum. Admission serum lead levels ranged from 54 to 72 micrograms/dl (normal, 0-30 micrograms/dl). Nonspecific neurologic manifestations consisted of dementia, diminished visual acuity, peripheral neuropathy, syncope, dizziness, nystagmus, easy fatigue, and back pain. Two patients developed chronic renal disease and hypertension; in both cases, serum parathormone was elevated. Blood, calcium, and phosphorus were normal in all three. No other structural abnormalities were observed with CT. Although the pathophysiologic mechanism of these findings remains poorly understood, it is suggested that chronic lead exposure should be included in the differential diagnosis of unexplained intracranial calcifications in adults.
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PMID:Intracranial calcification in adults with chronic lead exposure. 348 74

Using 31p-NMR (the phosphorus nuclear magnetic resonance) spectroscopy, we measured intracellular free Mg levels in the erythrocytes of untreated (n = 7) and diltiazem-treated spontaneously hypertensive rats (SHR) (n = 8), and compared them with age-matched Wistar-Kyoto rats (WKY) (n = 10). The intracellular free Mg levels were significantly (p less than 0.01) decreased in untreated SHR compared with those in control WKY. A successful antihypertensive treatment with diltiazem increased the intracellular free Mg levels compared with untreated SHR (p less than 0.05). Furthermore, an inverse correlation was observed between intracellular free Mg levels and blood pressure levels in all groups (r = -0.48, p less than 0.01, n = 25). These observations suggest that abnormalities of intracellular Mg metabolism may be, in part, related to the development or the maintenance of hypertension in SHR.
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PMID:Decreased intracellular free magnesium in erythrocytes of spontaneously hypertensive rats. 356 49

Increased interest in venous insufficiency has generated investigators to look for new insights to the pathophysiology of this disease. Previous clinical experience has revealed a relationship between venous hypertension and muscle atrophy in this group of patients. Phosphorous nuclear magnetic resonance studies has been done on a group of venous insufficiency patients to discover the biochemical changes.
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PMID:P31-NMR studies of muscle in patients with venous insufficiency. 362 54

Phosphorus-deficient diets fed to broiler chicks from day 1 to day 21 induced rickets. Some chicks were stunted, but most grew well, though they had increased respiratory rates, high arterial carbon dioxide partial pressure, and low oxygen partial pressure and were polycythemic. Most of the broilers that died showed signs of pulmocardiovascular abnormalities, some died from hypoxia, and some died from right ventricular failure with or without ascites. Many broilers had mild to marked right ventricular hypertrophy and dilation with or without ascites when examined at 21 days. It is suggested that right ventricular hypertrophy and dilation was a response to pulmonary arterial hypertension caused by chronic hypoxia, which resulted from inability to breathe normally because of poor rib strength and infolding. When right ventricular failure occurred, it was secondary to right ventricular hypertrophy and dilation.
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PMID:Right ventricular failure and ascites in broiler chickens caused by phosphorus-deficient diets. 376 7

It has been contended that the metabolism of vitamin D in spontaneously hypertensive rats (SHR) is different from that in Wistar-Kyoto rats (WKY). To investigate this possibility, the plasma concentration of 1,25-dihydroxycholecalciferol (1,25[OH]2D) and several known determinants of its production rate were measured in SHR and WKY given normal and restricted amounts of dietary phosphorus. In 12-week-old male SHR given a normal amount of dietary phosphorus, the mean plasma concentration of 1,25(OH)2D (72 +/- 5 pg/ml) was significantly lower than that in age-matched WKY (129 +/- 6 pg/ml; p less than 0.001). The lower plasma concentration of 1,25(OH)2D in the SHR could not be attributed to higher circulating levels of inorganic phosphorus or ionized calcium, lower plasma concentrations of 25-hydroxycholecalciferol, or acidosis. However, in the SHR, urinary excretion of cyclic adenosine 3',5'-monophosphate (12.5 +/- 0.4 nmol/mg creatinine) was significantly lower than that in WKY (15.2 +/- 0.3 nmol/mg creatinine; p less than 0.001). In both SHR and WKY, restriction of dietary phosphorus for 1 week induced an increase in the plasma concentration of 1,25(OH)2D without affecting blood pressure. The current findings indicate that in 12-week-old male SHR, 1,25(OH)2D metabolism is different from that in age-matched WKY. The activity of 25-hydroxyvitamin D-1 alpha-hydroxylase, however, appears to be at least partially responsive to short-term restriction of dietary phosphorus. In SHR, the activity of 25-hydroxyvitamin D-1 alpha-hydroxylase may be lower than that in WKY, perhaps due in part to some impairment in the renal metabolism of, or responsiveness to, cyclic adenosine 3',5'-monophosphate.
Hypertension 1986 Nov
PMID:Evidence for a difference in vitamin D metabolism between spontaneously hypertensive and Wistar-Kyoto rats. 377 Aug 64

Evidence from animal and human studies indicate that calcium supplementation may ameliorate two risk factors for atherosclerotic cardiovascular disease, hypertension and hyperlipidemia. We sought to characterize dietary fat consumption and plasma lipid profiles in hypertensive and normotensive subjects and plasma lipid responses to supplemental calcium. A randomized, double-blind, placebo-controlled, crossover protocol was used to assess blood pressure and lipid response to 8 wk of 1000 mg of elemental calcium in 43 hypertensive and 27 normotensive subjects. Nutrient intakes and plasma lipids were measured repeatedly. Hypertensive female subjects consumed significantly less (p less than 0.05) phosphorus, potassium, and magnesium and had significantly higher triglycerides (p less than 0.04) and lower HDL-cholesterol (p less than 0.02) than did normotensive subjects. There were no significant changes in dietary plasma lipids with calcium supplementation. Mildly hyperlipidemic normotensive subjects had a significant decrease in total cholesterol (p less than 0.05). No significant changes in plasma lipids occurred with calcium supplementation in hypertensive subjects.
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PMID:Plasma lipids and hypertension: response to calcium supplementation. 379 5

Associations between blood pressure and intakes of 61 dietary variables assessed by 24-h recall method were investigated in 615 men of Japanese ancestry living in Hawaii who had no history of cardiovascular disease or treated hypertension. Magnesium, calcium, phosphorus, potassium, fiber, vegetable protein, starch, vitamin C, and vitamin D intakes were significant variables that showed inverse associations with blood pressure in univariate and a multivariate analyses. Magnesium had the strongest association with blood pressure, which supports recent interest in its relation to blood pressure. Nevertheless, it was not possible to separate the effect of magnesium from that of other variables because of the problem of high intercorrelation among many nutrients. While recommendations based upon cross-sectional studies must be viewed cautiously, these results suggest that foods such as vegetables, fruits, whole grains, and low-fat dairy items are major sources of nutrients that may be protective against hypertension.
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PMID:Relationship of magnesium intake and other dietary factors to blood pressure: the Honolulu heart study. 381 46

Data from the first Health and Nutrition Examination Survey were analyzed with multivariate statistical techniques to determine whether there was evidence for a contributory role of alcohol in hypertension and to provide a suitable perspective on the importance of nutrient variables compared with other established risk factors for hypertension. The results of these analyses reaffirm the importance of alcohol and sodium intakes on blood pressures among US adults. Potassium (inversely) and phosphorus (directly) were also identified as important nutrient predictors of higher systolic blood pressure. Calcium intake was significantly related to systolic blood pressure only among nonwhite men and was not a significant predictor of systolic pressure overall. In addition, the results of the study reemphasized the paramount importance of age, race, and obesity in determining hypertension. Current nutrient intakes, by comparison, are relatively less important.
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PMID:Alcohol, nutrient intake, and hypertension in US adults. 397 35

The effects of prolonged bicuculline-induced seizures on cerebral blood flow and metabolism were determined in paralyzed, mechanically ventilated neonatal dogs. Transient changes occurring early in the course of status epilepticus included significant arterial hypertension, hypocarbia, elevation of plasma norepinephrine levels, and decline in brain glucose concentration. Cerebral blood flow remained elevated throughout the 45 minutes of seizure. Determination of cerebral metabolite values by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy and by in vitro enzymatic analysis of frozen brain samples showed significant decreases in the level of phosphocreatine and relatively less change in ATP values. Progressive intracellular acidosis occurred, coincident with elevation of brain lactate concentrations. We conclude that the physiological and metabolic alterations that occur during prolonged seizures are not uniform, but change with time. Any hypothesis advanced to explain the mechanism of neuronal injury during prolonged seizures must take into account these temporally related changes.
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PMID:31P NMR study of cerebral metabolism during prolonged seizures in the neonatal dog. 403 47


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