Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are common in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomerulosclerosis. We induced mesangial ferritin-antiferritin immune complex disease (FIC) in Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FIC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCl chow until 28 weeks of age. Groups of control S and R rats (no FIC) were either fed 0.3% NaCl for 28 weeks or switched to 8.0% NaCl chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age. R rats with or without FIC did not develop hypertension; mesangial injury was minimal. At 14 weeks of age, only S FIC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis. At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FIC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S FIC at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glomerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.
 ...
PMID:Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats. 623 58

Anionic groups on cerebral arteriolar endothelium were localized using cationized ferritin (CF), and alterations in the distribution of these groups were documented in arterioles with increased permeability to horseradish peroxidase (HRP) in angiotensin-induced acute hypertension. Normotensive animals showed a uniform distribution of anionic groups on the endothelial luminal plasma membrane when fixed or live vessels were reacted with CF. Anionic groups were localized at the mouth of pinocytotic vesicles in both preparations; however, only live cells demonstrated CF particles within vesicles, and the possibility that these represent pinocytosed CF particles cannot be ruled out. Cationized ferritin particles were not observed on the plasma membranes within interendothelial spaces in either of the preparations. Sixty percent of hypertensive animals with pressures over 200 mmHg showed increased arteriolar permeability to HRP. At 2.5 min, permeable arteriolar segments with active vesicular transport of HRP showed marked reduction or loss of CF binding. Capillaries and venules in the adjacent cortex and nonpermeable arterioles demonstrated linear endothelial CF binding similar to controls. Most permeable vessels of animals killed 6-20 min after onset of acute hypertension when the blood-brain barrier is usually closed showed CF binding on endothelium indicating that there is rapid restoration of the net negative charge. These studies demonstrate that increased arteriolar permeability in acute hypertension is associated with a transient alteration of surface charge. The mechanism by which charge is altered remains to be determined.
 ...
PMID:Cerebral endothelial surface charge in hypertension. 647 87

The effects of acute angiotensin II (AII) induced hypertension on renal hemodynamics, urinary excretory rates, and clearances of endogenous proteins, together with colloidal iron staining and numerical density of differently charged ferritins in glomerular basement membrane (GBM) have been studied. AII decreases para-aminohippurate clearance (63%) more than glomerular filtration rate (GFR) (42%), resulting in an increased filtration fraction (54%). Simultaneously, large increments in the excretory rates and clearances of albumin and IgG2a occur. The number of native ferritin particles per unit volume of GBM and its different layers increases significantly in both superficial and juxtamedullary glomeruli as a result of acute hypertension. In contrast, the number of cationized ferritin particles per unit volume of GBM as well as colloidal iron staining of GBM and adjacent cell membranes remain unchanged, irrespective of AII treatment. The results demonstrate that acute AII-induced hypertension enhances glomerular permeability to proteins of different size and shape in the absence of detectable alterations in the fixed negative charges of the GBM. Since both RBF and GFR are decreased, the increased transglomerular passage of proteins in acute hypertension appears to be due to an increase in the pore size of the glomerular filter, induced possibly by either high intracapillary pressure and/or a direct action of AII on GBM constituents.
 ...
PMID:Characterization of glomerular permeability and proteinuria in acute hypertension in the rat. 648 64

Acute hypertension induced by intravenous infusion of angiotensin II (AII) leads to enhanced transglomerular passage of albumin and IgG, as demonstrated by electronmicroscopic immunoperoxidase techniques. Although no morphological damage of the capillary wall was detected, significant amounts of macromolecules were present in the mesangial region. On a functional basis, a 42% decrease in glomerular filtration rate and a 63% decline in p-aminohippurate clearance were seen, resulting in a 54% increase in the filtration fraction. Quantitative measurements of albumin and IgG2a clearances showed a 90- and 15-fold increase, respectively. Similarly, the concentration of native ferritin particles in the glomerular basement membrane (GBM) increased 11-fold. On the other hand, the number of cationized ferritin particles and the staining properties of GBM to colloidal iron were not altered. These observations indicate that acute AII-induced hypertension affects glomerular permeability to proteins of different size and shape, possibly by increasing the pore size of the glomerular filter by either high intracapillary pressure and/or a direct action of AII on GBM constituents.
 ...
PMID:Glomerular permeability in acute hypertension. 654 34

A perfusion-fixation and vascular casting technique was used to assess the effects of acute, angiotensin-induced hypertension on the intrarenal arteries and, for comparison, the small arteries of the intestine. The first objective was to establish that the technique accurately preserves postmortem the vascular changes induced by acute hypertension. To do this, the easily accessible intestinal arteries were examined and photographed both in vivo and after fixation and injection of Batson's no. 17 casting resin in a group of angiotensin-treated rats and controls. The second objective was to apply the technique to observe and compare acute hypertensive changes in the intrarenal and intestinal arteries; studies included scanning electron microscopy of vascular casts and transmission electron microscopy of vessel walls using ferritin as a tracer to assess permeability. In the angiotensin-treated rats, casts of both intrarenal and intestinal arteries showed many well-defined zones of constriction and nonconstriction. Transmission electron microscopy of both the smaller intrarenal (interlobular) arteries and intestinal vessels revealed focal smooth muscle rarefaction and abnormal permeability to ferritin, found only in the nonconstricted zones. This study provides new evidence that in the kidney, as in the intestine, acute hypertension produces a characteristic pattern of arterial constriction and nonconstriction, and that hypertensive vascular lesions with accompanying increased permeability occur exclusively in the nonconstricted zones.
 ...
PMID:Effects of acute, angiotensin-induced hypertension on intrarenal arteries in the rat. 673 41

The experiment was designed to test whether the ability of heparin to prevent vascular "fibrinoid" necrosis in severe hypertension is related to its effects on vascular permeability. Hypertension was produced by infusion of angiotensin II into rats for 1 or 4 hours; some rats were treated with heparin and others not. Native ferritin was used as a tracer, and small arteries of the intestine were examined by light and electron microscopy. Rats not subjected to angiotensin II were used as controls. Half were treated with heparin, and half were not. Arteries from normotensive animals showed no signs of permeability to ferritin, damage to the vessel wall, or irregularities in caliber. Vessels from hypertensive rats had alternating zones of constriction and dilatation. Ferritin penetration and vessel wall damage were found only in dilated zones; these were focal in the 1-hour experiments and more extensive in the 4-hour experiments. No differences were observed between heparin-treated and non-heparin-treated rats with respect to permeability to ferritin or to vessel wall damage. However, in the 4-hour experiments, non-heparin-treated animals had occasional fibrinlike deposits at sites of severe medial damage; these were never found in heparin-treated animals. The findings suggest that although heparin does not appear to affect vascular permeability or medial damage during acute hypertension, it may prevent polymerization of fibrin in damaged vessel walls--presumably a result of the drug's anticoagulant properties.
 ...
PMID:The effects of heparin treatment on vascular permeability and vessel wall damage in acute hypertension in the rat. 685 20

Accelerated hypertension is a convenient model for studying the pathomechanism of hypertensive vascular lesions. It has not been settled, however, whether such lesions are really equivalent to those developing slowly in the course of experimental hypertensive vascular disease. In the present study, early vascular lesions of accelerated hypertension have been compared with those of hypertensive vascular disease by using two complementary techniques: small-molecule plasma-protein label (Ferrlecit) and a macromolecular tracer protein (horse ferritin). Two kinds of vascular lesions have been distinguished. Non-destructive vascular lesions exhibit necrotic smooth-muscle cells with intracellular deposition of Ferrlecit-labelled plasma proteins and intact basement-membrane barrier to the macromolecular tracer. Destructive vascular lesions, in turn, are characterized by the breakdown of the basement-membrane barrier to the macromolecular tracer. Incipient destructive lesions are identified as dissecting microaneurysms initiated by small ruptures of the basement membrane framework. Both non-destructive vascular lesions and incipient destructive vascular lesions end in confluent medial destruction that precedes the formation of fibrinoid necrosis. The localization and morphology of vascular lesions is identical both in hypertensive vascular disease and in accelerated hypertension. Circumstantial evidence strongly suggests that non-destructive vascular lesions are caused by arterial contraction. Nevertheless, the possibility that non-destructive lesions are but abortive forms of destructive ones cannot be excluded.
 ...
PMID:Morphogenesis of hypertensive vascular lesions. 717 73

Severe increases in blood pressure (BP) are associated with a segmental pattern of constriction and dilatation in small arteries and arterioles, but the pathogenesis is poorly understood. We showed that the isolated, perfused rabbit ear artery typically develops segmental constriction and dilatation when intraluminal pressure is > 160-180 mm Hg during field stimulation of perivascular nerves (> 6 Hz) or extra- or intraluminal infusions of norepinephrine (NE > 10(-7) M) or phenylephrine (PE) (> 5 x 10(-7) M). Light, transmission, and scanning electron microscopy showed that the dilated vessel segments initially show endothelial injury with no smooth muscle lesions. After repeated or prolonged exposure to high intraluminal pressure, dilated segments manifest extensive and severe endothelial and smooth muscle damage. Dilated regions also became abnormally permeable to tracer particles (ferritin). Constricted segments did not show evidence of endothelial or smooth muscle injury or hyperpermeability. These changes, i.e., segmental vasoconstriction/dilatation, hyperpermeability, and vessel wall damage localized to dilated segments, are comparable to those that occur in small arteries and arterioles during severe hypertension. We discuss the potential usefulness of the isolated ear artery as a model for studying the pathogenesis and morphology of segmental vasoconstriction/dilatation.
 ...
PMID:Isolated, perfused rabbit ear artery: a model for studying segmental vasoconstriction and dilatation. 751 24

Thalassaemia major determines an impaired effort tolerance because of a condition of severe anaemia, progressive left ventricular dysfunction, pulmonary circulation compromise. The aim of our study is to evaluate haemodynamic response to exercise in thalassaemic patients without clinical features of heart failure. We have selected 13 patients affected by thalassaemia major (Thal+; 10-18 years). Each patient was transfused when haemoglobin values were < 9-9.5 g/dl and was treated with desferrioxamine (40 mg/kg sc) when serum ferritin values were > 2,000 ng/ml. Thal+ patients were compared with normal subjects (Thal- 10-16 years). No patient assumed hypotensive therapy, no had familiar history of hypertension. Both groups have undergone an ergometric stress test at the cycloergometer, with increase of 25 W every 2 min, up to the reaching of the maximum age-related heart rate, or up to muscle exhaustion or unbearable dyspnea, followed by a 10 min recovery phase. The following parameters were taken in consideration: systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), the product of the heart rate by the systolic blood pressure (DP), at rest, at the maximum common work (MCW), at maximum stress and in the recovery phases. At rest, only DP showed significant differences between the two groups: in Thal+ patients higher than in Thal- (p = 0.045). At the MCW, Thal+ patients had SBP (p = 0.019), DBP (p = 0.01), HR (p = 0.035) and DP (p = 0.003) higher than Thal- patients. At maximum stress only DBP showed significant differences in Thal+ patients (p = 0.019), although Thal+ patients achieved lower levels of workload (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Cardiovascular adaptation to the stress test in subjects with Cooley's disease]. 780 70

The recombinant human erythropoietin (rHuEPO) by subcutaneous route has been considered the drug of choice for the correction of the anemia of chronic renal patients. PURPOSE--To evaluate the efficacy of a new preparation of rHuEPO in the correction of the anemia of chronic renal patients maintained by haemodialysis, exclusively administered by subcutaneous route, studying the adverse effects and searching for predictive factors for the response to this medication. METHODS--Twelve patients in regular haemodialysis were treated with freeze-dried rHuEPO by subcutaneous route during 18 months with initial doses of 20U/kg/dialysis. They were submitted to a careful clinical and laboratory monitoring for all this study. RESULTS--Eleven patients ended the study reaching the target hematocrit (Htc) of 30% and keeping it during the whole period of the study. The mean correction and maintenance doses of rHuEPO were 65U/kg/dialysis and 51U/kg/dialysis respectively. At the 12th week of the study a significative increase of Htc (18.4 +/- 3.5% vs. 25.4% +/- 3.8%, p < 0.05) was demonstrated. An increase of the erythrocytes and hemoglobin was concomitantly observed. Leucocytes and platelets increased significantly from the 24th week and kept steadily until the end of study. Just potassium increased in the biochemistry analysis of the patients at the 4th and the 12th week of the study returning to the basal values at the 24th week. The evolution of the iron metabolism parameters demonstrated an intermitent and statistically significant decrease of transferrin saturation at the 1st, 12th and 24th week, returning to the basal levels at the end of study. The serum ferritin did not change (582.7 +/- 700, 9ng/mL vs. 700.0 +/- 651, 6ng/nL). The weight and the blood pressure did not change either, although 2 normotensive patients became hypertensive and 2 others with controlled hypertension needed drug rearrange for blood pressure control (36%). A patient had a seizure episode with a full recovery. CONCLUSION--The rHuEPO has proved to be a safe and an efficient drug with easily controlled adverse effect.
 ...
PMID:[Correction of anemia in chronic kidney failure with lyophilized recombinant human erythropoietin using a subcutaneous approach]. 782 Jan 45


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