Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is first reported the hygienic epidemiological assessment of electrodialysis drinking water with multidiscipline methods including environmental epidemiology, toxicology, chemistry and clinical medicine. The results showed that the occurrence of malignant tumours in residents drinking electrodialysis water did not directly associate with their drinking water, we also did not find that there was any influence of electrodialysis water on residents' liver and gastrointestinal function, and the rate of thyroid enlargement, prevalence rates of dental fluorosis and dental caries as well as the level of saliva lysozyme in children. However, the morbidity rate of hypertension in the residents drinking electrodialysis water was higher than that in those drinking non-electrodialysis water.
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PMID:[Hygienic epidemiological assessment of electrodialysis drinking water]. 142 40

Neutrophilic granulocytes were exposed to an atmosphere of nearly 100% oxygen (hyperoxia) for one hour. The nitroblue tetrazolium (NBT) reduction, reflecting oxygen radical release, was decreased both in resting and stimulated cells, but lysozyme release was unchanged. Short time exposure of patients to oxygen hypertension might therefore be beneficial as therapy, in conditions where reduced production of oxygen radicals is required. The NBT reduction of resting and stimulated neutrophils in an atmosphere of purified argon (hypoxia) was also considerably decreased, and the lysozyme release unchanged. This reflects the anaerobic conditions in abscesses, where the contribution of neutrophil oxygen metabolites to the killing of microorganism might be reduced.
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PMID:Significance of oxygen availability for release of oxygen free radicals and lysozyme by neutrophils. 196 35

Lysozyme activity was measured in amniotic fluid samples from 90 pregnant women with gestational age ranging from 30 to 41 weeks. Twenty-nine samples were from high-risk subjects with different pathologies and signs of fetal distress. The control group consisted of 20 normal and 41 pathological pregnant women, whose disorders included Rh isoimmunization, diabetes, systemic arterial hypertension and pre-eclampsia without signs of fetal distress. Amniotic fluid lysozyme levels in normal controls were similar to those detected in abnormal pregnant women without signs of fetal distress (means = 156.0 vs 131.8 micrograms/ml for 34-37 weeks of gestation), with a tendency toward higher values as pregnancy progressed to term (means = 182.1 vs 155.4 micrograms/ml for 38-41 weeks of gestation). Lysozyme levels were significantly lower in high-risk pregnant women with signs of fetal distress, regardless of neonate birth weight, than in subjects showing no such signs (means = 40.3 and means = 25.4 micrograms/ml at 34-37 and 38-41 weeks of gestation, respectively). These data support the possibility of using amniotic fluid lysozyme activity levels as an indicator of fetal distress.
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PMID:Amniotic fluid lysozyme activity in fetal distress. 209 89

An investigation was carried out into renal injury caused by extracorporeal piezoelectric lithotripsy (EPL) using an EDAP lithotriptor. Four urinary proteins, with a molecular weight range of 160000-14500, immunoglobulin G (IgG), N-acetyl-beta-glucosaminidase (NAG), albumin and lysozyme, were monitored in 27 patients 1 day before and 1, 7, 30, 90 and 180 days after unilateral EPL treatment. All patients had non-obstructive renal stones, previously untreated. Apart from 5 patients with stablised hypertension and 6 with persistent urinary infections due to the infected stones, all patients appeared healthy, as confirmed by clinical, haematological and biochemical investigations. Only albumin levels increased significantly 1 day after treatment; statistically nonsignificant increases and decreases were recorded in the levels of NAG and lysozome respectively. IgG was beyond the limit of detection (less than 0.5 mg%) in all patients. The albumin level returned to normal 7 days after treatment. The EPL-induced increase in albumin was recorded in 88% of patients, compared with increased levels of NAG in 46% and lysozyme in 64%, mainly in those with infected stones. These findings indicated a transient glomerular injury after EPL treatment.
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PMID:Excretion of urinary protein induced by extracorporeal piezoelectric lithotripsy. 226 27

There is evidence that increased excretion of urinary enzymes and low-molecular mass proteins indicate impaired tubular function. The excretion of N-acetyl-beta-D-glucosaminidase (NAG), lysozyme, and ribonuclease in Type I diabetic patients with (n = 19) and without (n = 17) persistent proteinuria (urinary protein excretion greater than 0.5 g/day) was investigated and compared with this excretion in 30 weight- and gender-matched nondiabetic subjects without renal disease. Urinary NAG excretion was significantly higher in diabetic patients with and without persistent proteinuria (1.16 +/- 0.09 and 3.19 +/- 1.2 Umol/L creatinine, respectively) compared to controls (0.37 +/- 0.03 Umol/L creatinine p less than 0.01). In addition, the urinary excretion of lysozyme and ribonuclease was significantly increased in diabetic patients. Urinary NAG was found to correlate positively with albuminuria and proteinuria (r = 0.95 and 0.93, respectively), as well as with ribonuclease and lysozyme (r = 0.93 and 0.60; p less than 0.01) in patients with persistent proteinuria. Furthermore, NAG excretion was significantly related to the duration of diabetes (r = 0.36; p less than 0.05). No relationship existed between urinary NAG and serum creatinine, beta-2-microglobulin, and degree of metabolic control (HbA7). The lysozyme excretion, but not NAG excretion, was significantly related to hypertension in patients with clinical proteinuria. In conclusion, our results suggest a relationship between the development of tubular dysfunction and the impairment of glomerular function in diabetic nephropathy. An increased excretion of NAG and low-molecular mass proteins may indicate early nephropathy
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PMID:Further evidence for tubular dysfunction in insulin dependent diabetes. 252 61

In Goldblatt hypertension in rats produced by implanting a silver clip on the left renal artery, captopril induces a greater difference in the 1-min uptake of diethylenetriaminepentaacetic acid (DTPA) between the two kidneys than in baseline uptakes, similar to the experiences in unilateral renovascular hypertension in man. The combination of captopril and furosemide induces an even greater difference in renal uptakes than with captopril alone in this rat model. In paired experiments, DTPA complexes were used as a standard to compare the differences in renal uptake between the two kidneys after captopril-furosemide with other existing and potential renal radiodiagnostic agents. No statistically significant difference was found between DTPA, glucoheptonate, dimercaptosuccinic acid, aminated dextran, or lysozyme. However, the differences in renal uptake were significantly less with hippuran than with DTPA. Furosemide and captopril caused delayed renal retention of hippuran after one minute. This response appeared to be due to non-specific volume depletion because it occurred in both clipped and unclipped kidneys.
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PMID:Comparison of different radioactive agents for the detection of renovascular hypertension with captopril in a rat model. 328 Jul 51

In a 38-year-old woman, arterial hypertension was diagnosed a few weeks before her death. She died unexpectedly before a diagnostic clarification of the cause was possible. Autopsy revealed an arterial fibromuscular dysplasia with manifestation in both common iliac arteries, both renal arteries, the celiac trunk and the splenic artery. Both renal arteries displayed stenotic dissecant aneurysms which were the cause of the arterial hypertension. As a rare and lethal complication of fibromuscular dysplasia, a ruptured saccular aneurysm was found in the splenic artery. Histologically, the vascular alterations were a combination of medical fibromuscular dysplasia (type II) and periarterial or adventitial fibroplasia (type III). On the basis of the immunohistochemical detection of abundant lysozyme-positive cells, the periarterial fibroplasia appears to be a secondary chronic granulating and cicatricial reaction and not a separate form of fibromuscular dysplasia.
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PMID:[Arterial fibromuscular dysplasia as an unexpected cause of death in adults]. 367 85

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

We compared glucocorticoid receptor binding characteristics and glucocorticoid responsiveness of human mononuclear leukocytes (HML) from hypertensive patients and matched normotensive volunteers. We also considered associations of these variables with plasma renin activity, aldosterone, cortisol, corticotropin, and electrolyte concentrations. We calculated binding affinity (Kd; nmol/L) and capacity (Bmax; sites/cell) for dexamethasone and cortisol from homologous and heterologous competition curves for specific [3H]dexamethasone binding sites on HML isolated from the blood of normotensive volunteers and subjects with essential hypertension. Glucocorticoid responsiveness of HML was evaluated as IC50 values (nmol/L) for dexamethasone and cortisol for the inhibition of lysozyme release. We measured plasma hormones by radioimmunoassay. Kd values (mean+/-SE) for cortisol in HML of hypertensive patients were higher than in control subjects (24.6+/-2.4 versus 17.5+/-1.7 nmol/L, P<.04). Binding capacity (4978+/-391 versus 4131+/-321 sites/cell), Kd values for dexamethasone (6.7+/-0.5 versus 5.7+/-0.3 nmol/L), and IC50 values for dexamethasone (3.4+/-0.3 versus 3.1+/-0.2 nmol/L) and cortisol (12.2+/-1.6 versus 9.5+/-0.3 nmol/L) were not significantly different. Patients with renin values less than 0.13 ng angiotensin I/L per second were markedly less sensitive to cortisol than those with higher values. Both Kd (30.3+/-2.5 versus 19.2+/-2.4 nmol/L) and IC50 values (15.5+/-1.8 versus 8.9+/-1.2 nmol/L) for cortisol were significantly higher in patients with lower renin values (P<.03). Other variables, including plasma hormone and electrolyte values and binding characteristics for dexamethasone, were not different. These data suggest that cortisol binding to glucocorticoid receptor is slightly impaired in patients with essential hypertension. In vivo, this could lead to inappropriate binding of cortisol to mineralocorticoid receptors. Hence, decreased sensitivity to cortisol is associated with renin suppression. This hypothesis is supported by evidence of hypertension and low renin activity, which others have described in patients with primary glucocorticoid resistance due to mutations of the glucocorticoid receptor.
Hypertension 1997 Nov
PMID:Impaired cortisol binding to glucocorticoid receptors in hypertensive patients. 936 87

Intrauterine foetal growth retardation (IUGR) implies increased risk of morbidity and mortality of the newborn. Aetiology of intrauterine retardation is probably multifactorial and may include maternal infection, malnutrition, placental dysfunction, hypertension, toxaemia, smoking, professional and environmental exposure. The work concentrates on the lead, zinc and lysozyme levels in blood and placental tissues of 50 females in the IUGR group and 43 females from a control group. Statistically significant differences in zinc and lead levels between the compared group were found. The IUGR group had lower zinc and higher lead levels. A significant negative correlation of zinc and lead levels was observed. We found a statistically significant relationship between lead levels in placental tissues and the age of the pregnant women. Higher age is associated with higher lead levels in placental tissue, whereas zinc levels decrease. In placental tissues of pregnant females of the IUGR group higher lysozyme levels were found. On the basis of the discussed results the authors recommend zinc supplementation during the pregnancy.
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PMID:Relation between concentration of lead, zinc and lysozyme in placentas of women with intrauterine foetal growth retardation. 1008 21


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