(Na+, K+)-ATPase activity in a preparation from human post-mortem myocardium

Gibson, Keith; Harris, Peter

doi:10.1093/cvr/4.2.201

Cited by 15 publications

(11 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[31], however, failed to demonstrate any sodium transport inhibiting substances in uremic serum. On the other hand, ATP con centration is elevated in RBCs of uremics [4,23,27,42] and might result in an inhibition of Na-K-ATPase by excess substrate as previously reported [20]. Additionally the abnormal Km value of Na-K-ATPase for its substrate ATP [27] might also result in a diminished Na-K-ATPase activity thus impairing the utilization of ATP for active electrolyte transport as well.…”

Section: Discussionmentioning

confidence: 93%

Red Blood Cell Sodium Transport and Phosphate Release in Uremia

Walter¹,

Becht²

1983

Nephron

View full text Add to dashboard Cite

Red blood cell (RBC) phosphate release was linear for more than 1 h and dependent on the intracellular hydrolysis of organic phosphate esters. In uremics on chronic hemodialysis total phosphate release was significantly increased suggesting an elevated RBC energy metabolism. Ouabain-sensitive phosphate release, however, was decreased. For RBCs of controls and uremic subjects approximately 80% of inorganic phosphate liberated within the cell was recycled. Thus, RBC phosphate release represents 20% of intracellular phosphate ester metabolism. In uremia active electrolyte transport was diminished, suggesting an impaired Na-K-ATPase activity. It resulted in an increased RBC sodium and a decreased potassium concentration. The positive correlation between ouabain-sensitive rate constant for sodium efflux and ouabain-sensitive RBC phosphate release indicates that ouabain inhibition of phosphate elimination might be related to Na-K-ATPase. In RBCs of uremic subjects almost 4% of the increased energy metabolism was needed for active electrolyte transport mechanisms, in control RBCs 12% was required.

show abstract

Section: Discussionmentioning

confidence: 93%

Red Blood Cell Sodium Transport and Phosphate Release in Uremia

Walter¹,

Becht²

1983

Nephron

View full text Add to dashboard Cite

show abstract

“…The activity was greater in post-mortem renal tissue than in post-mortem myocardial tissue (Gibson & Harris, 1970a) and skeletal muscle (Samaha & Gergely, 1966) where average values of activity were found to be 5.4 and 10 pmol of Pi h-' mg of protein-' respectively. In the rat renal microsomal Na' ,K+-ATPase activity is also greater than cardiac (Gibson & Harris, 1970b).…”

Section: Discussionmentioning

confidence: 83%

“…Microsomal Na+,K+-ATPase activity from human post-mortem kidney possesses similar properties to that isolated from human heart muscle (Gibson & Harris, 1968, 1970a, skeletal muscle (Samaha & Gergely, 1966) and erythrocytes (Dunham & Glynn, 1961), although there are certain obvious differences. The activity was greater in post-mortem renal tissue than in post-mortem myocardial tissue (Gibson & Harris, 1970a) and skeletal muscle (Samaha & Gergely, 1966) where average values of activity were found to be 5.4 and 10 pmol of Pi h-' mg of protein-' respectively.…”

Section: Discussionmentioning

confidence: 86%

Distribution and Properties of Na+, K+-ATPase in Human Post-Mortem Kidney and the Effects of Diuretics

1972

Self Cite

View full text Add to dashboard Cite

show abstract

“…This suggests that there is still further activity of the enzyme in vivo. Gibson and Harris (1970) have reported low values for sodiumpotassium ATPase in human heart samples from post-mortem myocardium. These workers found that the activity of the cardiac microsomal sodium-potassium ATPase did not differ in patients dying from cardiac disease and those dying from other causes.…”

Section: Resultsmentioning

confidence: 95%

“…Microsomal-bound digoxin and sodium-potassium ATPase activity was determined as previously described (Goldman et al, 1973). In two patients digoxin in varying concentrations was incubated with the microsomal fraction containing (Na+, K+)-ATPase and (Mg ++)-ATPase at 37°C for 30 and 45 minutes respectively.…”

Section: Biochemical Methodsmentioning

confidence: 99%

Physiological Distribution of Digoxin in Human Heart

1975

Br Med J

View full text Add to dashboard Cite

SummaryUsing the recipient's human heart removed at cardiac transplantation, the distribution of digoxin at both the cellular and subcellular level has been studied. In the presence of diffuse histological myocardial abnormalities tissue digoxin is decreased, but the subcellular distribution, presumably reflecting binding to a possible receptor site, is uniform. When the histological abnormality is focal then digoxin distribution is uniform.These results suggest that in the presence of myocardial ischaemia plasma digoxin concentrations may not reflect total myocardial levels accurately.

show abstract

(Na+, K+)-ATPase activity in a preparation from human post-mortem myocardium

Cited by 15 publications

References 0 publications

Red Blood Cell Sodium Transport and Phosphate Release in Uremia

Red Blood Cell Sodium Transport and Phosphate Release in Uremia

Distribution and Properties of Na+, K+-ATPase in Human Post-Mortem Kidney and the Effects of Diuretics

Physiological Distribution of Digoxin in Human Heart

Contact Info

Product

Resources

About