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

Focal areas of recent and old necrosis are a consistent finding in brain in chronic hypertension. The possibility that areas represent foci of increased vascular permeability leading to chronic edema and tissue breakdown was investigated in the present study. Rats with chronic renal hypertension demonstrated increased cerebrovascular permeability in focal cortical areas throughout the 7-week period of study. Combined use of tracers and immunohistochemistry demonstrated that these areas of increased permeability with protein extravasation were of different ages. Stage I lesions showed protein in and around arteriolar walls with no cellular reaction indicating that these were very early lesions and corresponded to the findings using HRP as a tracer. Necrosis of the neuropil and an astrocytic and microglial response associated with diffuse collections of protein in the neuropil characterized stage II lesions. Stage III lesions consisted of glial scars or cystic spaces lined by astroglia and associated with absent or sparse protein deposits. Animals that died or were sick prior to killing and had diffuse cerebral edema showed large stage II cortical lesions associated with widespread serum protein extravasation into the white matter of both hemispheres. The principal mechanism resulting in the permeability alterations was enhanced pinocytotic transport of tracer across the endothelium of penetrating cortical arterioles. Vascular occlusion by thrombi was not observed in pial or intracerebral vessels. Our findings are consistent with the hypothesis that increased vascular permeability leads to chronic edema and tissue necrosis in chronic hypertension.
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PMID:Cerebral changes in chronic hypertension: combined permeability and immunohistochemical studies. 669 53

To test the role of central neurogenic factors in sodium-depleted states, cerebrospinal fluid (CSF) norepinephrine, epinephrine, and dopamine were measured in mongrel dogs first on a normal sodium intake (65 mEq sodium/day) and then on a 21-day regime of low sodium diet (4 mEq/day combined with diuretics). Plasma catecholamines were measured in the same group of dogs. Three weeks of sodium depletion supplemented with diuretics caused a 24-fold increase in plasma renin activity, hemoconcentration, and elevated serum protein concentration. Both plasma and CSF sodium decreased significantly. After sodium depletion, plasma norepinephrine rose 76% but epinephrine and dopamine did not change. The same pattern was observed whether samples were obtained in conscious or anesthetized animals. In CSF, norepinephrine rose 44% during sodium depletion, while epinephrine and dopamine remained unchanged. The CSF norepinephrine was related inversely to the CSF sodium concentration and directly to plasma renin activity. These observations support the view that the combined procedure of restricted dietary sodium intake and diuretic therapy causes alterations in CSF norepinephrine in a direction compatible with possible overactivity of central noradrenergic neurons.
Hypertension
PMID:Effect of chronic sodium depletion on cerebrospinal fluid and plasma catecholamines. 701 63

The 4 year prospective trial on the effectiveness of the antihypertensive treatment was performed in 100 mild hypertensive patients of the aged, the average age being 76.1 years. Dropouts during the drug-off control period were 9 cases. The matched pair group was selected by the age, sex, and blood pressure. Forty-four drug treated cases and 47 placebo treated cases were comparable in blood pressure as well as in laboratory data. Cerebrovascular and cardiac complications were observed in 4 cases or 10.5% in the drug group, and in 9 cases or 22.0% in the placebo group. When 8 cases of blood pressure elevation over 200/110 mmHg in the placebo group were added to the cardiovascular complications, dropouts in placebo group reached 41.5%, and this showed the significant difference. Other complications were observed in 12 cases or 31.6% in the drug group and in 17 cases or 41.5% in the placebo group. Major complications were cancers, infections, and bone or joint diseases. Blood pressure was decreased from 171/87 to 151/80 in the drug group, and the average decrease was 20/7 mmHg in 4 year period. No significant changes in hematocrit, serum protein, urea nitrogen, uric acid, sodium, and potassium were observed during the trial period. The present study suggested that antihypertensive treatment was effective in the aged with mild hypertension, and that careful follow up was needed not only for cardiovascular complications but also for general health condition.
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PMID:Prospective study on the treatment of mild hypertension in the aged. 701 98

1. To explore the effect of nephritis on development of genetic hypertension we immunized 10-week-old spontaneously hypertensive rats with purified rat kidney brush-border antigen. This induces Heymann nephritis (autologous immune complex nephritis), which does not elevate blood pressure in normal rats. 2. Nephritis developed in 11 of the 12 immunized animals, and systolic blood pressure rose to a significantly higher level than in the non-immunized spontaneously hypertensive rats within 4 weeks. Blood pressure remained higher in the immunized rats at 17 weeks, heart weights were greater, but creatinine clearance remained unchanged. 3. At 6 weeks, urinary sodium excretion was greater in the immunized spontaneously hypertensive rats, whereas at 17 weeks, sodium excretion was decreased in these animals along with reduced serum protein concentration, packed cell volume and plasma renin activity, as compared with that of the controls. 4. Development of hypertension in nephritic rats, therefore, appeared unrelated to sodium excretion; signs of volume expansion emerged later. 5. Acceleration of the development of spontaneous hypertension by Heymann nephritis, also leading to sustained higher blood pressure levels than in spontaneously hypertensive rats, offers a new approach to experimental study of immune mechanisms behind acceleration of pre-existing hypertension. This may have important bearings on essential hypertension as well.
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PMID:Aggravation of hypertension in spontaneously hypertensive rats by Heymann nephritis. 723 40

To clarify the natural history of IgA nephropathy and to determine important factors in the progressive loss of renal function in affected patients, 121 patients with IgA nephropathy were followed for a median of 92 months. The cumulative probability of not progressing to end-stage renal failure (that is, of renal survival) was 0.87 at 15 years after the onset of 1st symptoms and 0.86 at 10 years after presentation and biopsy. Eight percent of patients progressed to end-stage renal failure, and 12% had a greater than 20% decline in renal function. A complete remission of disease activity was seen in 12% of patients, and the remaining 68% maintained stable renal function. When the final serum creatinine was expressed as a percentage of the initial serum creatinine for each patient and compared with all other variables, a number of factors were found to affect renal outcome. Of the presenting features, increased age, family history of nephritis, longer duration of symptoms, and presence of either nephrotic-range proteinuria or hypertension were all associated, by univariate analysis, with an adverse outcome, while a history of recurrent macroscopic hematuria and infection-associated exacerbations of disease activity were associated with a favorable outcome. Multivariate analysis showed that nephrotic-range proteinuria had an independent adverse effect. Of the initial laboratory findings, by univariate analysis, the number of hyaline casts, the degree of impairment of renal function, the degree of proteinuria, raised beta globulins on serum protein electrophoresis, and serum C4 concentrations were all associated with an adverse outcome, while the severity of initial hematuria and pyuria were associated with a favorable outcome. Renal biopsy findings associated with an adverse outcome by univariate analysis include, on light microscopy, the percentage of glomeruli with global sclerosis or segmental sclerosis or adhesions, the degrees of tubular atrophy or interstitial fibrosis, interstitial inflammation and blood-vessel thickening, and, on immunofluorescence, the intensity of IgA deposition. Multivariate analysis showed independent adverse effects on renal outcome of global glomerulosclerosis, segmental glomerulosclerosis or adhesions, and a combined mesangial and capillary wall deposition of IgM. Features at final assessment or during follow-up associated with an adverse outcome include, by univariate analysis, the number of hyaline casts, the degree of impairment of renal function, the degree of proteinuria, reduced serum IgG and IGM concentrations, reduced final IgA expressed as a percentage of the initial IgA concentration, transient decreases of creatinine clearance during follow-up of > 10% or > 20%, and persistence or development of hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:IgA nephropathy: analysis of the natural history, important factors in the progression of renal disease, and a review of the literature. 815 67

We investigated the hemodynamic, renal, and hormonal effects of cyclosporin A (CyA) treatment (6 mg/kg per day) for 4 weeks in 12 patients with nephrotic syndrome (8 women: 4 men, aged 36-66 years, 3 cases of focal glomerular sclerosis: 9 cases of membranous nephropathy). To evaluate the effects of CyA on the diurnal variation of blood pressure (BP), 24-h non-invasive BP monitoring was performed using model ABPM-630 (Nihon Colin, Tokyo, Japan) before and during CyA treatment. As indices of hemodynamics, intra-arterial pressure was monitored and cardiac output was measured by the dye-dilution technique using a cuvette at 0 and 4 weeks after treatment. CyA ameliorated urinary protein excretion and hypoproteinemia from 3.5 +/- 0.9 to 2.2 +/- 0.7 g/day, and serum protein concentration from 4.9 +/- 0.2 to 5.5 +/- 0.2 g/dl after 4 weeks' treatment. Endogenous creatinine clearance, 24-h urinary sodium excretion, and plasma renin activity decreased significantly at 1 week. CyA treatment raised casual BP from 122 +/- 4/75 +/- 2 to 140 +/- 5/87 +/- 3 mmHg after 1 week and to 146 +/- 4/90 +/- 2 mmHg after 4 weeks. Before treatment 24-h ambulatory BP monitoring showed BP reduction at night (116 +/- 5/68 +/- 3 mmHg) compared to the daytime (124 +/- 5/75 +/- 2 mmHg). The diurnal variation of BP disappeared during CyA treatment; mean daytime and nighttime pressures were 135 +/- 4/81 +/- 2, 132 +/- 5/80 +/- 3 mmHg at 1 week and 139 +/- 5/83 +/- 3, 131 +/- 6/80 +/- 3 mmHg at 4 weeks, respectively. On hemodynamic study; a 4-week treatment with CyA increased mean arterial pressure from 91 +/- 3 to 104 +/- 3 mmHg, total peripheral resistance index from 2.1 +/- 0.1 to 2.5 +/- 0.1 x 10(3) dyne.sec.cm-5.m2, and unchanged heart rate and cardiac index. Serum Mg concentration decreased from 2.1 +/- 0.1 to 1.7 +/- 0.1 mg/dl. These results suggest that CyA-induced hypertension is characterized by the loss of nocturnal decline in blood pressure, which is accompanied by volume retention after 1 week and systemic vasoconstriction after 4 weeks.
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PMID:[Effects of cyclosporin A on the diurnal variation of blood pressure in patients with nephrotic syndrome]. 919 62

Binswanger's disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we describe BBB dysfunction and its regional differences in the brains of Binswanger's disease patients. Twelve brains from Binswanger's disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, Clq and fibrinogen, both in the periventricular WM and subcortical WM in 5 out of 12 (42%) Binswanger's disease brains. These results indicate that WM lesions in Binswanger's disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension.
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PMID:Blood-brain barrier dysfunction in Binswanger's disease; an immunohistochemical study. 945 25

The prevalence of microalbuminuria and its relationship to cardiovascular disease risk factors were examined in subjects participating in an annual physical and laboratory examination program. The urinary albumin concentration and the urinary albumin/creatinine ratio were determined in morning urine specimens. A turbidimetric immunoassay was used for the measurement of urinary albumin. Of the 731 subjects, 41 (5.6%) who were weakly positive or positive on a routine dipstick test for protein were excluded from the final analysis of data. Microalbuminuria was present in 14.5% of the men, in 12.4% of the women, and in 13.2% of the entire subject population when defined as a urinary albumin concentration of 30-299 microgram/ml. The prevalence of microalbuminuria was significantly higher in subjects with a high normal blood pressure (15.0%) or hypertension (26.2%) as compared with normotensive subjects (6.5%). Subjects with impaired glucose tolerance (24.3%) or hyperglycemic subjects (50.0%) had a significantly higher prevalence of microalbuminuria than normoglycemic subjects (11.3%). The prevalence of microalbuminuria was significantly higher in subjects with left ventricular hypertrophy (47.1%) as compared with those with normal electrocardiograms (11.3%). A good correlation was observed between urinary albumin concentration and albumin/creatinine ratio, and both showed a significant positive correlation with age, systolic and diastolic blood pressures, and fasting plasma glucose, total serum protein, albumin, and triglyceride levels, but not with angiotensin-converting enzyme activity. Multiple regression analysis demonstrated that both the urinary albumin concentration and the albumin/creatinine ratio show a significant positive correlation with systolic blood pressure and fasting plasma glucose. The prevalence of microalbuminuria was about 13% in this Japanese cohort, and the systolic blood pressure and the fasting plasma glucose level were demonstrated as independent risk indicators for both urinary microalbumin level and urinary microalbumin/creatinine ratio.
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PMID:Prevalence of microalbuminuria and relationship to the risk of cardiovascular disease in the Japanese population. 1008 44

Despite improvements in dialysis therapy, the mortality rate of patients with end stage renal disease (ESRD) has remained high. A relatively high proportion of uremic patients dies within one year after the initiation of dialysis treatment. The aim of this study was to evaluate predictors for this early mortality in patients with ESRD. A total of 66 uremic patients were included in the study. Patients were divided in those who survived < 1 year (n = 17) and those who survived > or = 1 year (n = 49). We compared the prevalence of diabetes and hypertension and of vascular diseases as well as the prevalence of heart insufficiency (EF < 30%) and left ventricular hypertrophy (LVH). Additionally, we estimated the laboratory parameters serum creatinine, creatinine clearance, BUN, cholesterol, triglycerides, fibrinogen, serum protein, serum albumin and hemoglobin, and evaluated the indications for the initiation of dialysis therapy in both patient groups. The patients with survival < 1 year were significantly older (64+/-12 vs. 54+/-14 years, p<0.01) and showed a lower BMI (22+/-3 vs. 25+/-3, p<0.01) than those who survived > 1 year. The prevalence of diabetes (70% vs. 31%, p<0.05), cardiac insufficiency (70% vs. 16%, p<0.025), cardiovascular disease (65% vs. 28%, p<0.05) and peripheral vascular diseases (70% vs. 28%, p<0.05) was significantly higher in the patients with early mortality. The prevalence of hypertension was similar in both groups, however, the prevalence of LVH was significantly higher in the patients who survived < 1 year (88% vs. 37%, p<0.05). Laboratory parameters were not significantly different in the two groups of patients, with the exception of serum albumin, which was significantly lower in the patients with early mortality (3.5+/-0.6 vs. 3.9+/-0.4 g/l, p<0.02). Hyperhydration was the most common indication for the start of dialysis in patients with early mortality (59% vs. 13%, p<0.025). Cardiac insufficiency was the most common cause of death in these subjects (n = 10, 59%). Six individuals (12%) died within four weeks after initiating dialysis therapy. Thus, there are several predictors for early mortality in end-stage renal disease patients, including high age, low BMI, the presence of diabetes, coronary heart disease, heart insufficiency and LVH, as well as low serum albumin levels. A relatively high percentage of patients die shortly after the start of dialysis therapy. Heart insufficiency is the most common cause of early death in these patients.
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PMID:Predialysis management and predictors for early mortality in uremic patients who die within one year after initiation of dialysis therapy. 1207 93

Changes in serum protein levels are produced by oral contraceptives. They reflect hepatic synthesis of proteins. Changes range from a 40% decrease in orosomucoid to an 180% increase in ceruloplasmin. Alterations in the concentration of some globulin proteins lead to altered serum levels of some hormones and trace metals. Plasma levels of cortisol and thyroxine are most affected. An estrogen-induced increase in thyroxine-binding globulin causes a transient reduction in free thyroxine (T4). This results in a compensatory increase in thyroid-stimulating hormone. The net effect is an unchanged concentration of T4 and the patient may be reported as euthyr id. Increases in renin substrate with rise in renin activity, angiotensin 2, and aldosterone, may be related to the development of hypertension in some women. Oral contraceptives may cause significant increases in some lipids. Elevations in cholesterol and nonesterified fatty acids are less changed. The drug-induced changes can complicate a definite diagnosis of hyperlipidemia. The glucose tolerance curve in users of oral contraceptives may simulate the diabetic type. Hepatic function tests may suggest hepatic damage. There is a higher incidence of cholecystitis and gallstones in women using oral contraceptives. Blood coagulation tests may be modified. Drug interference from oral contraceptive use must be considered in interpreting laboratory reports.
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PMID:Drug interference with laboratory tests: oral contraceptives. 1226 Jan 55


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