sodium/potassium pump sites were 43154 + 8037 molecules/cell (n = 25) in lymphocytes and 75474 ± 6764 (n = 9) molecules/cell in mixtures of mononucleated cells.5 Direct determination of the [3H]-ouabain binding capacity of lymphocytes can be performed with acceptable accuracy and precision using 30 ml whole blood. Provided high cell purity, this method may be useful, when studying sodium/potassium pump function in clinical settings.
The effect of captopril has been investigated in four patients with Bartter's syndrome treated for 12 weeks. Baseline biochemistry showed normal serum aldosterone (mean 347 pmol.l-1) and a mean serum renin of 217 mU-l-1, and a considerable increase in serum renin during captopril treatment. Serum aldosterone decreased gradually during the study period to about half its initial value. The patients presented with a mean serum potassium of 2.5 mmol.l-1, which rose to 3.4 mmol.l-1 on captopril. Lymphocytes showed a substantial captopril-induced increase in intracellular sodium (from 15 to 22.5 mmol.l-1 on average), but no change in the potassium content. Captopril was well-tolerated. It may be an alternative to potassium-sparing diuretics for maintaining normal serum potassium levels in patients with Bartter's syndrome.
Bartter's syndrome is characterized by chronic hypokalaemia, activation of the renin-angiotensin system and normal blood pressure. To investigate whether a generalized disturbance of sodium-potassium pump function might be of pathogenetic importance, lymphocytic sodium-potassium homeostasis was examined in 5 patients suffering from Bartter's syndrome. Two of the patients were treated with potassium chloride supplementation, the others were without medical treatment when studied. All were severely hypokalemic (serum potassium 2.8 \ m=+-\0.24 mmol/l, mean \ m=+-\ sem). Lymphocyte sodium and potassium concentration (14.4 \ m=+-\ 0.37 and 94.4 \ m=+-\ 7.7 mmol/l, respectively), ouabain sensitive 22Na-efflux rate constant (2.68 \ m=+-\ 0.25 h \ m=-\ 1) , and absolute ouabain sensitive efflux rate (38.16 \ m=+-\ 4.2 mmol \m=.\ 1\ m=-\ 1 \m=.\ h\m=-\1) did not differ from matched controls. Ouabain binding capacity was 126 900 \ m=+-\ 235000 sites/cell in the patients vs 50400 \ m=+-\ 17900 in controls (p <0.05). In conclusion, patients with Bartter's syndrome may have an intrinsic abnormal pump function, characterized by an increased pump density and a low cation turn-over rate per pump unit.
Lymphocytes were used as a cellular model for the in vitro measurements of maximal ouabain binding sites in order to assess any changes in young men at increased risk of developing essential hypertension, and to analyse whether any such changes were associated to borderline hypertension and/or heredity. Four groups were evaluated; 28 normotensive (NTO) and 20 borderline hypertensive (BHO) offspring of hypertensives. Twelve borderline hypertensives (BH) and 28 normotensive subjects (NT) with normotensive parents. The number of ouabain binding sites were significantly increased in the borderline hypertensives irrespective of heredity. The borderline hypertensives were heavier than the normotensives. A stepwise multiple regression model was therefore used in order to control confoundings by body mass index (BMI) and other factors such as age, gamma glutamyl transferase, 24 h sodium excretion, serum triglyceride, and serum cholesterol, which may influence the number of ouabain binding sites. Only BMI entered the stepwise model. These results indicate the presence of an increased number of sodium-potassium pumps in lymphocytes from borderline hypertensives. This difference may be attributed to the blood pressure disease or increased body mass.
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