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.

scholarly journals In vivo cation transport during short-term and long-term digoxin therapy.

1986 ◽  
Vol 22 (1) ◽  
pp. 27-30
Author(s):  
NA Boon ◽  
SE Pugh ◽  
KF Hallis ◽  
JK Aronson ◽  
DG Grahame-Smith
Keyword(s):  
Cation Transport ◽  
Short Term ◽  
Digoxin Therapy

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.

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

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.

Impaired prolactin response to arginine infusion and insulin hypoglycaemia in chronic renal failure

1983 ◽  
Vol 102 (4) ◽  
pp. 486-491 ◽  
Author(s):  
O. Schmitz ◽  
J. Møller
Keyword(s):  
Growth Hormone ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Elevated Level ◽  
Matched Control ◽  
Chronic Haemodialysis ◽  
Arginine Infusion ◽  
Pituitary Dysfunction ◽  
Prolactin Response ◽  
Insight Into

Abstract. The elevated level of circulating prolactin present in the majority of uraemic patients on chronic haemodialysis is primarily due to hypothalamic pituitary dysfunction. So far this defect has been illustrated by demonstration of a blunted prolactin response to TRH and failure of l-dopa to suppress prolactin levels. In the present study two powerful prolactin and growth hormone stimuli, namely iv arginine infusion and insulin hypoglycaemia were applied in a group of uraemic patients on chronic haemodialysis and in age matched control subjects. The prolactin increments to arginine infusion (4.4 ± 1.2 ng/ml vs 17.6 ± 4.6 ng/ml, mean ± se) and to insulin hypoglycaemia (7.9 ± 1.7 ng/ml vs 31.5 ± 5.4 ng/ml) were significantly suppressed in the uraemic patients compared to the controls (P < 0.05). In contradistinction the growth hormone rise provoked by the tests were similar in the two groups. Our results provide further insight into the hypothalamic pituitary derangement in uraemic patients and confirm the presumption of an insensitivity of the lactotrophs to stimulation in uraemic patients.

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.

scholarly journals Evaluation of the Relationship between Early Troponin Clearance and Short-Term Mortality in Patients with Chronic Renal Failure

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Ahmet Ozbek ◽  
Abdullah Algın ◽  
Gokhan Tas ◽  
Mehmet Ozgur Erdogan
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Survival Rates ◽  
Structural Heart Disease ◽  
Lactate Clearance ◽  
Acute Injury ◽  
Short Term ◽  
Survival Group ◽  
Parametric Data ◽  
Short Term Mortality

Objective. In patients with CKD, cTn concentrations may be elevated in the absence of AMI, which is a predicted finding caused by chronic structural heart disease rather than acute injury. The increase in troponin level observed in noncardiac conditions provides conflicting results when predicting mortality. Low lactate clearance was associated with increased mortality. Lactate clearance is calculated as follows: (early lactate − late lactate/early lactate) ∗ 100. We aimed to investigate whether troponin clearance calculated according to this formula had an effect on short-term mortality. Methods. The study included 300 patients with chronic renal failure who had a sepsis-related organ failure assessment (SOFA) score ≥3. By taking the baseline troponin at the time of emergency presentation as reference and comparing them with the fourth-hour troponin values, troponin clearance was investigated in the evaluation of mortality among hospitalized patients with CKD within the first month after discharge. The data obtained were analyzed using the SPSS data analysis software version 20.0. Student’s t-test was used for the parametric data, and the Chi-squared test for the nonparametric data. Results. Of the 300 patients evaluated, 189 patients survived (mean age 66.20 ± 14.597 years), and 111 died (mean age 74.81 ± 12.916 years). Troponin clearance was detected in 40 of the 111 patients in the mortality group and 119 of the 189 patients in the survival group. Troponin clearance was significantly more frequent in surviving patients (P=0.0000083). Conclusion. Troponin clearance can be considered as a valuable leading indicator of survival, but higher levels of troponin clearance did not lead to higher survival rates.

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