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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Na+,K+-ATPase concentration in rat cerebral cortex was studied by vanadate-facilitated [3H]ouabain binding to intact samples and by K+-dependent 3-O-methylfluorescein phosphatase activity determinations in crude homogenates. Methodological errors of both methods were evaluated. [3H]Ouabain binding to cerebral cortex obtained from 12-week-old rats measured incubating samples in buffer containing [3H]ouabain, and ouabain at a final concentration of 1 × 10–6 mol/L gave a value of 11,351 ± 177 (n = 5) pmol/g wet weight (mean ± SEM) without any significant variation between the lobes. Evaluation of affinity for ouabain was in agreement with a heterogeneous population of [3H]ouabain binding sites. K+-dependent 3-O-methylfluorescein phosphatase activity in crude cerebral homogenates of age-matched rats was 7.24 ± 0.14 (n = 5) μmol/min/g wet weight, corresponding to a Na+,K+-ATPase concentration of 12,209 ± 236 pmol/g wet weight. It was concluded that the present methods were suitable for quantitative studies of cerebral cortex Na+,K+-ATPase. The concentration of rat cerebral cortex Na+,K+-ATPase showed ∼10-fold increase within the first 4 weeks of life to reach a plateau of ∼11,000–12,000 pmol/g wet weight, indicating a larger synthesis of Na+,K+ pumps than tissue mass in rat cerebral cortex during the first 4 weeks of development. K+ depletion induced by K+-deficient fodder for 2 weeks resulted in a slight tendency toward a reduction in K+ content (6%, p 〉 0.5) and Na+,K+-ATPase concentration (3%, p 〉 0.4) in cerebral cortex, whereas soleus muscle K+ content and Na+,K+-ATPase concentration were decreased by 30 (p 〈 0.02) and 32% (p 〈 0.001), respectively. Hence, during K+ depletion, cerebral cortex can maintain almost normal K+ homeostasis, whereas K+ as well as Na+,K+ pumps are lost from skeletal muscles.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 175-181 
    ISSN: 1573-7241
    Keywords: Na ; K-ATPase ; 3H-ouabain binding ; specific digoxin Fab ; digitalis glycosides ; skeletal muscle ; digitalization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aims of the present study were to evaluate in humans the putative importance of skeletal muscle digitalis glycoside receptors (Na,K-ATPase) in the volume of distribution of digoxin and to assess whether therapeutic digoxin exposure might cause digitalis receptor upregulation in skeletal muscle. Samples of the vastus lateralis were obtained postmortem from 11 long-term (9 months to 9 years) digitalized (125–187.5 µg daily) and eight undigitalized subjects. In intact samples from digitalized patients, vanadate-facilitated3H-ouabain binding increased 15% (p〈0.02) from 150±18 to 173±13 pmol/g wet wt. (mean ± SEM) after clearing receptors of bound digoxin by washing samples in excess specific digoxin antibody fragments.3H-ouabain binding in the untreated group was 257±28 and 274±26 pmol/g wet wt. (7%, p〉0.30) before and after washing in specific dogoxin antibody fragments, respectively. Thus, the present study indicates a ~13% occupancy of skeletal muscle digitalis glycoside receptors with digoxin during digitalization. In light of the large skeletal muscle contribution to body mass, this indicates that the skeletal muscle Na,K-ATPase pool constitutes a major volume of distribution for digoxin during digitalization. The results gave no indication of skeletal muscle digitalis glycoside receptor upregulation in response to digoxin treatment. On the contrary, there was evidence of significantly lower (37%, p〈0.005) digitalis glycoside receptor concentration in the vastus lateralis of the digitalized patients, which may be of importance for skeletal muscle incapacity in heart failure.
    Type of Medium: Electronic Resource
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