These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Glucocorticoid-induced alterations in the sodium potassium pump of the human erythrocyte. Author: Kaji DM, Thakkar U, Kahn T. Journal: J Clin Invest; 1981 Aug; 68(2):422-30. PubMed ID: 6267104. Abstract: To evaluate the effects of glucocorticoids on the Na-K pump in human subjects, were evaluated the intracellular sodium and potassium, 42K influx across and the [3H]ouabain binding to cell membranes of intact human erythrocytes from a group of subjects taking glucocorticoids and a group of normal subjects. Intracellular sodium concentration was lower (7.2 +/- 0.4 vs. 10.9 +/- 0.2 mmol/liter cell water) and intracellular potassium concentration higher (149.8 +/- 1.5 vs. 137.2 +/- 1.2 mmol/liter cell water) in erythrocytes from steroid-treated patients. In spite of a significantly decrease intracellular sodium which normally diminishes ouabain-sensitive 42K influx, the ouabain-sensitive K influx was unchanged in erythrocytes from the steroid-treated group. Maximum [3H]ouabain binding was markedly higher in the steroid-treated group (835 +/- 44 vs. 449 +/- 11 sites/cell). There was close linear correlation between [3H]ouabain binding and inhibition of K pump, suggesting the specificity of ouabain binding to Na-K pump sites on the cell membrane. Association kinetics for ouabain were similar in the two groups despite the marked difference in the amount of [3H]ouabain binding. External potassium concentration required for half-maximum ouabain-sensitive K influx was identical in the two groups. Thus, the additional Na-K pump sites in the steroid-treated group were qualitatively similar to those in normals. These results suggest that administration of glucocorticoids leads to an increase in the number of Na-K pump sites. The increase in the number of Na-K pump sites may explain the low levels of intracellular sodium and higher cell potassium observed in steroid-treated subjects.[Abstract] [Full Text] [Related] [New Search]