In Vivo Evidence of Reduced Cation Transport in Chronic Renal Failure

1983 ◽  
Vol 65 (3) ◽  
pp. 60P-60P
Author(s):  
N.A. Boon ◽  
A.E. Raine ◽  
K.F. Hallis ◽  
C.M. Perkins ◽  
D.G. Grahame-Smith ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cation Transport

Cation transport abnormalities in vivo in untreated essential hypertension

1986 ◽  
Vol 70 (6) ◽  
pp. 611-616 ◽  
Author(s):  
Nicholas A. Boon ◽  
Jeffrey K. Aronson ◽  
Keith F. Hallis ◽  
David G. Grahame-Smith
Keyword(s):  
Renal Failure ◽  
Essential Hypertension ◽  
Chronic Renal Failure ◽  
Oral Administration ◽  
Matched Control ◽  
Cation Transport ◽  
Short Term ◽  
Sodium Potassium ◽  
Digoxin Therapy

1. In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations after the oral administration of rubidium chloride. 2. In this paper we describe our findings in 22 patients with untreated essential hypertension, compared with the findings in 22 carefully matched control subjects. Our findings in patients receiving short-term digoxin therapy and in patients with chronic renal failure are also included for comparison. 3. Whereas the findings in patients receiving digoxin and in patients with chronic renal failure are compatible with a widespread reduction in sodium, potassium-ATPase activity in vivo, the findings in patients with untreated essential hypertension are not. 4. Further analysis of the data and a similar study of the disposition of 42K after the intravenous administration of 42KC1 suggest that in vivo net cation transport is enhanced in the erythrocytes of patients with untreated essential hypertension.

A Method for the Study of Cation Transport in vivo: Effects of Digoxin Administration and of Chronic Renal Failure on the Disposition of An Oral Load of Rubidium Chloride

1984 ◽  
Vol 66 (5) ◽  
pp. 569-574 ◽  
Author(s):  
N. A. Boon ◽  
J. K. Aronson ◽  
K. F. Hallis ◽  
N. J. White ◽  
A. E. G. Raine ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cation Transport ◽  
The Body ◽  
Control Group ◽  
Loading Dose ◽  
Rubidium Chloride ◽  
Body Tissues

1. In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations following an oral load of rubidium chloride. The changes in plasma rubidium concentration are related to the distribution of rubidium to all the body tissues and the changes in intra-erythrocytic rubidium concentrations provide an example of rubidium uptake by one particular tissue. 2. In eight healthy volunteers pretreatment with a loading dose of digoxin (20 μg/kg) enhanced the rise in plasma rubidium concentrations and attenuated the rise in intra-erythrocytic rubidium concentrations after the oral load of rubidium chloride. 3. Ten patients with chronic renal failure, compared with a well-matched control group, were found to have changes similar to, but more marked than, those caused by digoxin, i.e. a much greater rise in plasma rubidium concentrations and a much smaller rise in intra-erythrocytic rubidium concentrations, after the oral load of rubidium chloride. 4. These findings are consistent with widespread reduction in Na+,K+-ATPase activity in subjects who have taken a loading dose of digoxin and patients with chronic renal failure. They are, therefore, consistent with the findings of previous studies in vitro and show that it is possible to demonstrate changes in cation transport in vivo.

Effects of Haemodialysis and Continuous Ambulatory Peritoneal Dialysis on Abnormalities of Ion Transport in vivo in Patients with Chronic Renal Failure

1993 ◽  
Vol 85 (6) ◽  
pp. 725-731 ◽  
Author(s):  
Christopher J. Brearley ◽  
Jeffrey K. Aronson ◽  
Nicholas A. Boon ◽  
Anthony E. G. Raine
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Rate Constant ◽  
Cation Transport ◽  
Rubidium Uptake ◽  
Control Subjects ◽  
Pump Activity

1. We have studied Na+/K+ pump activity in vivo in three groups of subjects: patients with chronic renal failure not receiving maintenance dialysis, patients being treated by either haemodialysis or continuous ambulatory peritoneal dialysis, and matched control subjects. 2. To do this we have measured the changes in plasma and intraerythrocytic rubidium concentrations after an oral load of rubidium chloride, having previously shown that changes in the disposition of rubidium measured in this way reflect changes in the activity of the Na+/K+ pump in vivo. 3. Erythrocyte rubidium uptake was significantly reduced both in ten patients with chronic renal failure not receiving maintenance dialysis and in 12 patients being treated by haemodialysis, when compared with 31 healthy control subjects. In contrast, erythrocyte rubidium uptake was not altered in 13 patients treated by continuous ambulatory peritoneal dialysis. There was also a significantly reduced rate constant for erythrocyte rubidium uptake in patients with undialysed chronic renal failure (0.66 h−1) and in those treated by haemodialysis (0.78 h−1), whereas in patients treated by continuous ambulatory peritoneal dialysis the rate constant for erythrocyte rubidium uptake was not significantly different from control values (1.36h−1 and 1.41 h−1, respectively). 4. These findings are consistent with a reversal of the inhibition of erythrocyte Na+/K+ pump activity in vivo found in chronic renal failure by continuous ambulatory peritoneal dialysis, but not by haemodialysis. This difference may be due to the failure of haemodialysis to clear a circulating inhibitor of Na+, K+-ATPase or to the rapid re-accumulation of such an inhibitor after haemodialysis. Alternatively, it could be due to a dialysable inhibitor of potassium efflux, with a secondary reduction in the activity of the Na+/K+ pump. 5. Neither continuous ambulatory peritoneal dialysis nor haemodialysis reversed the abnormal disposition of rubidium in the plasma found in undialysed patients. This suggests that the putative inhibitor which accumulates in chronic renal failure does not affect cation transport in all tissues of the body, and that abnormalities of cation transport in chronic renal failure may be due to more than one mechanism.

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.

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.

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

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.

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.

scholarly journals Renal synthesis of arginine in chronic renal failure: In vivo and in vitro studies in rats with 5/6 nephrectomy

1993 ◽  
Vol 44 (4) ◽  
pp. 676-683 ◽  
Author(s):  
Nadine Bouby ◽  
Christine Hassler ◽  
Philippe Parvy ◽  
Lise Bankir
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
In Vitro Studies
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