Endogenous vasopressin regulates Na-K-ATPase and Na+-K+-Cl− cotransporterrbsc-1 in rat outer medulla

2002 ◽  
Vol 282 (2) ◽  
pp. F265-F270 ◽  
Author(s):  
Claudia A. Bertuccio ◽  
Fernando R. Ibarra ◽  
Jorge E. Toledo ◽  
Elvira E. Arrizurieta ◽  
Rodolfo S. Martin
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atpase Activity ◽  
Receptor Antagonist ◽  
The Other ◽  
Outer Medulla ◽  
Physiological Conditions ◽  
Increased Activity ◽  
Expression And Activity

Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V2-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 ± 1.5 to 3.7 ± 0.8 in controls ( P < 0.05) and from 19.0 ± 0.8 to 2.9 ± 0.5 μmol Pi · mg protein−1 · h−1 in moderate CRF rats ( P < 0.05). CRF was associated with a significant increase in Na-K-ATPase activity ( P < 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 ± 21.5% compared with controls ( P < 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 ± 9.5 and 105.3 ± 10.9%, respectively ( P < 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 ± 6.5 and 30.0 ± 6.9%, respectively ( P < 0.05), and was not influenced by CRF (95.7 ± 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.

Evidence for an Increased Generation of Prostacyclin in the Microvasculature and an Impairment of the Platelet α-Granule Release in Chronic Renal Failure

1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Clotting ◽  
Normal Subjects ◽  
Chronic Uraemia ◽  
Wall Interaction ◽  
End Stage ◽  
Granule Release

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.

scholarly journals Standardization of a method to study angiogenesis in a mouse model

2013 ◽  
Vol 85 (4) ◽  
pp. 1483-1487
Author(s):  
DAVID FEDER ◽  
FABIO F. PERRAZO ◽  
EDIMAR C. PEREIRA ◽  
SILVANA FORSAIT ◽  
CECILIA K.R. FEDER ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Animal Models ◽  
The Other ◽  
In Vivo Studies ◽  
Specific Method ◽  
Test Results ◽  
Hemoglobin Content ◽  
Physiological Conditions ◽  
Adult Organism

In the adult organism, angiogenesis is restricted to a few physiological conditions. On the other hand, uncontrolled angiogenesis have often been associated to angiogenesis-dependent pathologies. A variety of animal models have been described to provide more quantitative analysis of in vivo angiogenesis and to characterize pro- and antiangiogenic molecules. However, it is still necessary to establish a quantitative, reproducible and specific method for studies of angiogenesis factors and inhibitors. This work aimed to standardize a method for the study of angiogenesis and to investigate the effects of thalidomide on angiogenesis. Sponges of 0.5 x 0.5 x 0.5 cm were implanted in the back of mice groups, control and experimental (thalidomide 200 mg/K/day by gavage). After seven days, the sponges were removed. The dosage of hemoglobin in sponge and in circulation was performed and the ratio between the values was tested using nonparametric Mann-Whitney test. Results have shown that sponge-induced angiogenesis quantitated by ratio between hemoglobin content in serum and in sponge is a helpful model for in vivo studies on angiogenesis. Moreover, it was observed that sponge-induced angiogenesis can be suppressed by thalidomide, corroborating to the validity of the standardized method.

scholarly journals Familial Atypical Hemolytic Uremic Syndrome with Positive pS1191L (c.3572C> T) Mutation in CFH A Single-Center Experience

2019 ◽  
Author(s):  
Fadime ERSOY DURSUN ◽  
Gözde YESIL ◽  
Hasan DURSUN ◽  
Gülşah SASAK
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Family History ◽  
Hemolytic Uremic Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Gene Mutations ◽  
Factor H ◽  
The Other ◽  
History Of ◽  
Uremic Syndrome

Abstract Background: Atypical hemolytic uremic syndrome is a condition characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury, which can exhibit a poor prognosis. Gene mutations play a key role in this disease, which may be sporadic or familial. Methods: We studied, 13 people from the same family were investigated retrospectively for gene mutations of familial atypical hemolytic uremic syndrome after a patient presented to our emergency clinic with atypical hemolytic uremic syndrome and reported a family history of chronic renal failure. Results: The pS1191L mutation in the complement factor H gene was heterozygous in 6 people from the family of the patient with atypical hemolytic uremic syndrome. One of these people was our patient with acute renal failure and the other two are followed up by the Nephrology Clinic due to chronic renal failure. The other 3 persons showed no evidence of renal failure. The index case had a history of 6 sibling deaths; two of them died of chronic renal failure. Plasmapheresis and fresh frozen plasma treatment was given to our patient. When patient showed no response to this treatment, eculizumab therapy was started. Conclusions: The study demonstrated that a thorough family history should be taken in patients with atypical hemolytic uremic syndrome. These patients may have familial type of the disease and they should be screened genetically. Eculizumab should be the first choice in the treatment with plasmapheresis. It should be kept in mind that the use of eculizumab as prophylaxis in post-transplant therapy is extremely important for prevention of rejection.

Hyperprolactinemia as a Marker of Neurotransmitter Imbalance in Uremic Population

1987 ◽  
Vol 10 (4) ◽  
pp. 245-257 ◽  
Author(s):  
S. Biasioli ◽  
G. D'Andrea ◽  
G. Micieli ◽  
M. Feriani ◽  
D. Borin ◽  
...  
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Major Change ◽  
Serum Prolactin ◽  
Endogenous Opiates ◽  
Dopaminergic Activity ◽  
Dopaminergic Systems ◽  
Increased Activity

Serum prolactin (PRL) levels are elevated in patients with chronic renal failure (CRF) but the mechanisms responsible for these abnormalities are not fully understood. PRL secretion is undoubtedly influenced by many substances, which can be variously altered in uremia: monoamines, endogenous opiates and PTH. Our data suggest that in early renal failure PRL levels are already significantly high and the 24-h pattern of PRL secretion is significantly different from that in controls. PRL derangements could be due in mild renal failure, to unknown factors (GABA?); in severe CRF, to a major change in dopaminergic activity; in hemodialysis (HD), to a low turnover of monoamines, and in peritoneal dialysis (PD) to increased activity of sero-toninergic and dopaminergic systems.

scholarly journals Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra

2019 ◽  
Vol 39 (3) ◽  
pp. 186-191
Author(s):  
Marcos C. Sant’Anna ◽  
Guilherme F. Martins ◽  
Karina K.M.C. Flaiban ◽  
Luiz G.C. Trautwein ◽  
Maria I.M. Martins
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Injury ◽  
Renal Damage ◽  
Systemic Disease ◽  
The Other ◽  
Control Group ◽  
Creatinine Ratio ◽  
Renal Lesions ◽  
Tubular Cells

ABSTRACT: Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.

In-vivo induction of monocyte chemotactic and activating factor in patients with chronic renal failure

1995 ◽  
Vol 10 (12) ◽  
pp. 2244-2249 ◽  
Author(s):  
T. Akahoshi ◽  
N. Kobayashi ◽  
S. Hosaka ◽  
N. Sekiyama ◽  
C. Wada ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
In Vivo Induction

scholarly journals In vitro production of interleukin-1 receptor antagonist in chronic renal failure, CAPD and HD

1992 ◽  
Vol 42 (6) ◽  
pp. 1419-1424 ◽  
Author(s):  
Brian J.G. Pereira ◽  
Debra D. Poutsiaka ◽  
Andrew J. King ◽  
James A. Strom ◽  
Geetha Narayan ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Receptor Antagonist ◽  
Interleukin 1 ◽  
In Vitro Production ◽  
Interleukin 1 Receptor Antagonist ◽  
Vitro Production

Increased Inward Passive Permeability in Vitro to Sodium in Uraemic Erythrocytes

1996 ◽  
Vol 90 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Dalila B. Corry ◽  
Charma C. Ellis ◽  
Michael L. Tuck
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cytosolic Calcium ◽  
Na Efflux ◽  
The Mean ◽  
86Rb Influx ◽  
Cell Defect ◽  
External K

1. We have reported a normal sodium (Na) pump, but decreased loop-diuretic-sensitive Na efflux in erythrocytes from patients with chronic renal failure on haemodialysis, suggesting a different mode of co-transport in uraemia. 2. The present work extends these findings and examines in vitro simultaneous unidirectional and radiolabelled Na and K fluxes through the Na/K/Cl co-transport and the Na/K pump in washed erythrocytes from seven subjects with chronic renal failure and seven controls. Erythrocyte cytosolic calcium was also examined. 3. Ouabain-sensitive 86Rb influx was similar in patients and controls (1.76 ± 0.19 versus 1.72 ± 0.13 mmol h−1 litre−1 of erythrocytes) as was ouabain-sensitive 22Na efflux (3.62 ± 0.36 versus 4.04 ± 0.39 mmol h−1 litre−1 of erythrocytes). 4. Bumetanide-sensitive 86Rb and 22Na influx and 22Na efflux were measured at three concentrations (4, 8 and 12 mmol/l) of external K. In chronic renal failure, mean bumetanide-sensitive 22Na efflux was decreased at all external K concentrations compared with controls, and at physiological concentrations (4 mmol/l) external K was lower than controls (0.14 ± 0.01 versus 0.38 ± 0.05 mmol h−1 litre−1 of erythrocytes, P < 0.01). Mean bumetanide-sensitive 86Rb influx was also reduced in chronic renal failure at all external K concentrations, and at 4 mmol/l external K was lower than controls (0.13 ± 0.04 versus 0.34 ± 0.04 mmol h−1 litre−1 of erythrocytes, P < 0.01). Conversely, bumetanide-sensitive 22Na influx was markedly increased at all external K levels in chronic renal failure, and at 4 mmol/l external K values were elevated compared with controls (0.64 ± 0.18 versus 0.34 ± 0.04 mmol h−1 litre−1 of erythrocytes, P < 0.001). The mean cytosolic calcium concentration was higher in erythrocytes in chronic renal failure than controls (134.4 ± 8.6 versus 63.7 ± 5.8 nmol/l, P < 0.001). 5. Thus, in washed erythrocytes incubated in artificial media there is a markedly increased ouabain-insensitive Na influx in subjects with chronic renal failure which might be explained in part by the higher levels of cytosolic calcium. In vivo, this cell defect combined with suppression of the Na/K pump could lead to intracellular Na accumulation and play a role in uraemic complications.

scholarly journals Significance of lipoprotein(a) in diabetic chronic renal failure

2017 ◽  
Vol 5 (9) ◽  
pp. 3856
Author(s):  
Vasanthan M.
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Disease ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
The Other ◽  
Lipoprotein A ◽  
Positive Correlation ◽  
Duration Of Diabetes

Background: Diabetes mellitus, is a metabolic disease with an alarming prevalence worldwide. When uncontrolled, this can result in diseases such as chronic renal failure by various atherogenic factors including lipoprotein(a). Aim was to estimate the level of lipoprotein(a) in diabetic chronic renal failure patients and to correlate with healthy controls.Methods: 30 non-diabetic subjects and 30 diabetic CRF patients were included in the study. Lipoprotein(a) was estimated by immunoturbidimetric method and the other parameters by their respective methods in biochemistry auto-analyzer.Results: It was found from the study that there is a positive correlation of lipoprotein(a) levels with the duration of diabetes and was progressive with the diabetic complications.Conclusions: Lipoprotein(a) is responsible for atherogenic events in CRF patients.

Role of nitric oxide resistance in erythropoietin-induced hypertension in rats with chronic renal failure

1996 ◽  
Vol 271 (1) ◽  
pp. E113-E122 ◽  
Author(s):  
N. D. Vaziri ◽  
X. J. Zhou ◽  
F. Naqvi ◽  
J. Smith ◽  
F. Oveisi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Magnesium Concentration ◽  
Induced Hypertension ◽  
Group A

We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). After partial nephrectomy, rats were randomized into four groups. Group A received EPO, 150 U/kg, two times weekly for 6 wk to prevent anemia; group B received placebo injections and became anemic; group C received EPO but was kept anemic by dietary iron deficiency; and group D received placebo and regular transfusions to match hematocrit (Hct) in group A. Blood pressure (BP), Hct, platelet cytosolic calcium ([Ca2+]i) and magnesium concentration, and pressor and vasodilatory responses were determined. By design, Hct in groups A and D were comparable and significantly greater (P < 0.01) than in groups B and C. Despite divergent Hct values, the EPO-treated groups A and C showed a significant rise in BP compared with the placebo-treated groups B and D. HTN occurred whether EPO therapy was begun immediately or 4 wk after nephrectomy. EPO therapy augmented the elevation of basal [Ca2+]i and restored the defective thrombin-mediated rise of platelet [Ca2+]i in CRF animals. EPO therapy did not alter caudal artery contraction in response to either 68 mM K(+)-induced depolarization, angiotensin II or alpha 1-agonist, methoxamine in vitro, or the pressor response to angiotensin II in vivo. However, EPO therapy impaired the hypotensive response to nitric oxide (NO) donors, sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine, and reversed the CRF-induced upregulation of guanosine 3',5'-cyclic monophosphate production by thoracic aorta in vitro. Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO.

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