The influence of a low-potassium diet on rat-erythrocyte-membrane adenosine triphosphatase

Chan, Phillip C.; Sanslone, William R.

doi:10.1016/0003-9861(69)90249-5

Cited by 41 publications

(8 citation statements)

References 8 publications

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“…In cells grown in the protein synthesis inhibitor cycloheximide, the number of pumps decline at a rate of 2 % h -after a 3 h lag (Lamb, Boardman, Newton & Aiton, 1973;Aiton, 1976;Lamb & Ogden, 1982a): in cells grown in low K or high serum concentrations, a cycloheximide-sensitive increase in pump numbers occurs at rates of 5 and 10%h-1 respectively (Boardman, Huett, Lamb, Newton & Polson, 1974;Aiton, 1976): in cells grown in ouabain and then returned to normal medium a cycloheximide-sensitive recovery starts at 6 h and occurs at a rate of 7% h-1 . Similar results on net changes in other cells have been reported by Chan & Sanslone (1969) in rat red blood cells, and by Fletcher, Stainer & Holmes (1967) in duck nasal glands. Membrane proteins in liver cells turnover at rates of about 2 % h (Dean, 1978).…”

Section: Introductionsupporting

confidence: 89%

The effects of chloroquine and other weak bases on the accumulation and efflux of digoxin and ouabain in HeLa cells

Griffiths

Lamb

Ogden

1983

British J Pharmacology

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Section: Introductionsupporting

confidence: 89%

The effects of chloroquine and other weak bases on the accumulation and efflux of digoxin and ouabain in HeLa cells

Griffiths

Lamb

Ogden

1983

British J Pharmacology

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“…This has also been found in other laboratories [7,11] in human red cells and also in rat erythrocytes [9]. This increase in (Na + +K+)-ATPase activity in chronic potassium depletion is also seen in guinea pig myocardial tissue [12], and in rabbit heart [30] but apparently not in rat soleus muscle [26,27].…”

Section: Discussionsupporting

confidence: 82%

Influence of digitalis and diuretics on ouabain binding sites on human erythrocytes

1984

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It has been reported that during chronic treatment with digitalis, the number of digitalis binding sites is increased in human erythrocytes [22]. From this finding a tachyphylaxis for cardiac glycosides has been postulated. We reinvestigated this problem in several groups of patients. The number of 3H-ouabain binding sites per erythrocyte in control persons (group I) was 214 +/- 60, n = 43 (means +/- SD). The dissociation constant (KD) was 1.8 +/- 0.5 nM. Thirteen patients (group II) taking cardiac glycosides only, for at least 6 months, had 281 +/- 99 (p less than 0.05) ouabain binding sites per single red cell, KD = 1.8 +/- 0.7 nM. Group III (34 patients) took digitalis for more than 6 months and diuretics for at least 3 months (352 +/- 126 (p less than 0.001), KD = 1.6 +/- 0.6). Twenty-three of these (group IV) were taking a combination with "K+-saving" diuretics (336 +/- 194 (p less than 0.01), KD = 1.6 +/- 0.5) and (group V, 11 patients) a combination with "K+-losing" diuretics (462 +/- 133 (p less than 0.001), KD = 1.4 +/- 0.4). Nine patients (group VI) had a chronic hypokalemia, mainly due to taking furosemide (437 +/- 98 (p less than 0.001), KD = 1.5 +/- 0.4). Four control persons took 50 mg hydrochlorothiazide daily for more than 4 months without measurable K+-losses and without changes in ouabain binding sites. It is concluded from these findings that diuretic treatment with chronic hypokalemia in addition to digitalis is accompanied by a significant increase in ouabain binding sites in human red cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Membrane (Na+, Kt-activatedj-A'Tf'ase activity was increased by 130% in the left ventricle of chronically K +-depleted guinea pigs (Erdmann et al, 1971) probably as a result of a quantitative increase in enzyme. A similar increase in membrane ATPase activity was found in the erythrocytes of chronically K +-depleted rats (Chan & Sanslone, 1969) and these erythrocytes did not lose intracellular K + during depletion. HeLa and Girardi cells (Boardman, Lamb & McCall, 1972) grown in a low K+ culture medium develop an increase in ouabain-binding sites.…”

Section: Discussionsupporting

confidence: 78%

Effect of Chronic Dietary Potassium Depletion and Repletion on Cardiac and Skeletal Muscle Structure, Electrolytes and pH in the Rabbit

Hall

Cameron

1981

Clinical Science

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1. Chronic dietary potassium depletion which was severe enough to decrease skeletal muscle intracellular potassium concentration by 20%, did not significantly reduce cardiac intracellular potassium concentration of rabbits. 2. Chronic potassium depletion caused a fall in intracellular pH in skeletal muscle, but no changes occurred in cardiac intracellular pH. 3. Intracellular potassium was increased above normal after 1 week of potassium repletion, but had returned to normal after 3 weeks of repletion. This may have resulted from potassium retaining mechanisms which had developed during depletion and which persisted during the early stages of repletion. 4. Cardiac and skeletal muscle from potassium-depleted animals did not show any structural damage when examined by light and electron microscopy.

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The influence of a low-potassium diet on rat-erythrocyte-membrane adenosine triphosphatase

Cited by 41 publications

References 8 publications

The effects of chloroquine and other weak bases on the accumulation and efflux of digoxin and ouabain in HeLa cells

The effects of chloroquine and other weak bases on the accumulation and efflux of digoxin and ouabain in HeLa cells

Influence of digitalis and diuretics on ouabain binding sites on human erythrocytes

Effect of Chronic Dietary Potassium Depletion and Repletion on Cardiac and Skeletal Muscle Structure, Electrolytes and pH in the Rabbit

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