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C Guarena

Publications and source records attributed to C Guarena.

33 records · Page 2Linked to original sources
PubMed1988

Abnormalities of sodium transport by sodium, potassium-activated adenosine triphosphatase in erythrocytes from obese children.

1. Intracellular Na+ concentration [Na+]i and Na+ extrusion catalysed by sodium potassium-activated adenosine triphosphatase (Na+, K+-pump) were evaluated in erythrocytes from 21 obese children and 20 normal weight- and age-matched controls. 2. Obese children showed a significantly decreased Vmax. for Na+, K+-pump-mediated Na+ efflux (5638 +/- 338 vs 7597 +/- 335 mumol h-1 litre-1 of cells mean +/- SEM, P = 0.01), while [Na+]i (9.3 +/- 0.3 vs 9.1 +/- 0.5 mmol/litre of cells, mean +/- SEM, NS) and Na+ efflux in fresh cells (2380 +/- 153 vs 2533 +/- 180 mumol h-1 litre-1 of cells, mean +/- SEM, NS) were similar in both groups. 3. Mean diastolic blood pressure was significantly higher in obese children than in controls, although both groups were normotensive (73.8 +/- 1.3 vs 66.2 +/- 1.9 mmHg, mean +/- SEM, P = 0.009). 4. Abnormal Na+, K+-pump activity is present in individuals with idiopathic obesity. 5. The possible link between obesity and blood pressure regulation may be mediated through modifications in Na+,K+-pump activity.

Adolescent↗
PubMed1988

Pathogenesis of arterial hypertension in chronic uraemia: the role of reduced Na,K-ATPase activity.

In 38 uraemic dialysed patients (17 normotensive, 21 hypertensive) we measured (1) erythrocyte sodium concentration [Nai] and ouabain-sensitive sodium efflux, and (2) arterial pressure, cardiac index and total peripheral resistance. Erythrocyte Na-K pump activity was lower in hypertensive than in normotensive patients (P less than 0.02). Hypertensive patients had significantly higher peripheral resistance than normotensive patients (P less than 0.05), while the cardiac index was similar in both groups. Inverse correlations were found between the rate constant for ouabain-sensitive sodium efflux in erythrocytes and both systolic and diastolic pressure (r = -0.43 and r = -0.45, respectively; P less than 0.01) and total peripheral resistance (r = -0.76; P less than 0.0001). Our data suggest that reduced sodium transport by the Na-K pump plays a role in the pathogenesis of arterial hypertension in patients with chronic uraemia.

Blood Pressure↗
PubMed1985

Evaluation of ouabain-insensitive red blood cell cation transport in uremic patients.

The authors present the results of a simultaneous assay of: intracellular Na+ and K+ concentrations, Na+ and K+ outward bumetanide-sensitive effluxes (Na+, K+ cotransport), Na+ efflux stimulated by extracellular Li+ (Na+, Li+ countertransport), and ouabain- and bumetanide-resistant Na+ and K+ effluxes (passive membrane permeability) performed in red blood cells from 15 uremic patients an regular hemodialysis and from 12 normal subjects, with an established flux assay. Na+ and K+ effluxes by the Na+, K+ cotransport system were significantly (p less than 0.01) lower in uremic patients then in normals (219 +/- 37 vs 82 +/- 17 mumol/l RBC/h and 251 +/- 29 vs 139 +/- 14 mumol/l RBC/h respectively). In normal subjects the bumetanide sensitive Na+ and K+ effluxes were strongly (r = 0.89; p less than 0.01) intercorrelated; and the intracellular Na+ concentration was related to the outward Na+ cotransport flux (r = 0.53; p approximately 0.05). Among uremic patients these correlations were not found. Na+ and K+ intracellular concentrations, passive Na+ and K+ permeability, and Na+, Li+ countertransport activity were not different among uremic patients and normal controls. In conclusion, in uremic dialyzed patients, red blood cell Na+, K+ cotransport activity is quite uniformly suppressed. The possible pathogenesis of this disfunction is still speculative and deserves further studies.

Adult↗
PubMed1985

Effects of an intravenous saline load on erythrocyte sodium transport in normal human subjects.

The effects of a 2 litre intravenous infusion of saline (0.9% NaCl solution) over 3 h on erythrocyte transmembrane sodium transport were studied in 12 normal human subjects. After saline infusion a significant (P less than 0.01) reduction of both outward Na+,K+ pump- and Na+,K+ cotransport-mediated Na+ effluxes was observed. The Na+,Li+ countertransport rate and the passive Na+ permeability did not change. The incubation of the subjects' erythrocytes, obtained on a separate occasion, with their own plasma taken after the saline infusion, induced an inhibition of both Na+,K+ pump and Na+,K+ cotransport outward sodium fluxes. The percentage decrease after incubation was closely correlated with the percentage reduction induced by the saline infusion in vivo (r = 0.93 for the pump and r = 0.96 for cotransport; P less than 0.01). These data suggest that extracellular fluid volume expansion affects the release of circulating factors modulating sodium transport by the Na+,K+ pump and by Na+,K+ cotransport.

Adult↗
PubMed1985

Acute effects of hemodialysis on erythrocyte sodium fluxes in uremic patients.

The acute effects of both acetate and bicarbonate hemodialysis on erythrocyte transmembrane sodium fluxes were investigated in 15 patients with chronic uremia. We observed a significance (p less than 0.01) stimulation of the Na+,K+ pump in both procedures, with a significant correlation to the amount of fluid removed during hemodialysis (r = 0.56, p less than 0.03). Outward Na+ cotransport fluxes significantly rose (p less than 0.05) after acetate hemodialysis and decreased (p less than 0.05) after bicarbonate hemodialysis. Minor and not significant pre- and posthemodialysis bidirectional changes were observed as regards the intraerythrocyte Na+ and K+ concentration, passive Na+ and K+ permeability, and Na+,Li+ countertransport. Hemodialysis may acutely affect the erythrocyte sodium pump and cotransport fluxes, possibly through the modulation of hormonal factors triggered by the extracellular volume changes.

Acetates↗
PubMedDate not supplied

[Effects of saline infusion on the activity of erythrocyte sodium-potassium pump in normal subjects and in patients with essential hypertension].

The effects of a 2 litre isotonic saline infusion on erythrocyte Na,K pump activity and urinary sodium excretion (UNaV) were evaluated in 20 patients with essential hypertension and 15 normotensive subjects. The effect of preincubation of normal erythrocytes in plasma from hypertensive patients on erythrocyte Na,K pump was also studied. Before saline infusion no significant differences were found between normotensive and hypertensive subjects in the mean values of intracellular sodium and potassium concentration, ouabain-sensitive Na efflux in erythrocytes and urinary sodium excretion. Erythrocyte Na,K pump activity decreased significantly (p less than 0.01) after saline infusion in both groups of subjects. The reduction was significantly lower in hypertensives than in normotensive. delta UNaV was significantly higher in hypertensive patients than in normotensive subjects (25 +/- 4 vs 14 +/- 2 mmol/h; p = 0.04). Only in normal subjects a significant correlation was found between the difference in Na,K pump activity pre and post saline infusion and delta UNaV (r = 0.52; p less than 0.05). Plasma from hypertensive patients obtained before saline infusion significantly (p less than 0.01) inhibited Na,K pump of erythrocytes from normal subjects; plasma taken after saline infusion produced a marked increase of this inhibition, significantly (p less than 0.01) higher than serum taken before the infusion.

Adult↗
PubMedDate not supplied

[Changes in cellular ion transport and arterial pressure in renal transplant recipients undergoing cyclosporin treatment].

Arterial hypertension is a common side effect of cyclosporine A (CyA). Aim of the study was to evaluate the activity of erythrocyte (RBC) Na transport in two groups of patients with a well functioning renal graft (Crs less than 1.7 mg/dl) treated by prednisone+azathioprine (10 pts), or prednisone+CyA (21 pts), in relationship with blood pressure status. Twenty-one age matched healthy subjects were studied as a control group. Na,K pump and Na,K cotransport were significantly lower in CyA than in AZA patients (2,184 +/- 106 vs 3,089 +/- 162 and 58 +/- 8 vs 187 +/- 28 mumol/l RBC/h: p less than 0.01), without differences between normotensive and hypertensive patients. Na,K pump efflux in normal subjects was 2334 +/- 66 mumol/l RBC/h (p less than 0.01 vs AZA), NA,K cotransport was 205 +/- 18 mumol/l RBC/h (p less than 0.01 vs CyA). Significant correlations were found between RBC Na,K pump activity and trough plasma CyA levels (p less than 0.02) and between systolic pressure and plasma creatinine in CyA patients (p less than 0.01). Trough plasma CyA levels were higher in hypertensive than in normotensive CyA patients (64 +/- 5 vs 46 +/- 4 ng/ml; p less than 0.01).

Adult↗
PubMedDate not supplied

[Biofiltration without buffering substances in the dialysate].

A new hemodiafiltration technique, acetate free biofiltration (AFB), has been recently introduced in the treatment of chronic uremia. It is performed with a buffer free dialysate and a simultaneous infusion in post-dilution mode of a sodium bicarbonate solution (concentration 145-166 mEq/l; infusion rate 1.2-2 l/h). A polyacrylonitrile hollow fiber AN69 HF 1.2 sqm dialyzer is employed. In acute studies pCO2 remains stable throughout the treatment, as well as pCO2. We have found a significant inverse correlation between delta[HCO3-] pre and post treatment and basal [HCO3-] (r = -0.88; p less than 0.001), with an excellent correction of uremic acidosis, avoiding post dialytic alkalosis. Our long term experience on 6 patients followed up to 31 months, allows us to consider AFB as a feasible and safe treatment, offering a good correction of uremic acidosis and an excellent hemodynamic tolerance. We propose AFB as a competitive technique with respect to bicarbonate hemodialysis, hemodiafiltration and standard biofiltration.

Acidosis↗