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Dexamethasone-induced sodium influx in human lymphocytes
M Tepel1, G Theilmeier, C Teupe
1Medizinische Universitäts-Poliklinik, University of Münster, Germany.
Insights
Dexamethasone, a glucocorticoid, increases intracellular sodium in human lymphocytes, likely through early genomic effects influencing sodium transport across the cell membrane.
Area of Science:
- Endocrinology
- Cell Biology
- Molecular Pharmacology
Background:
- Glucocorticoids are potent regulators of cellular function.
- Intracellular sodium concentration ([Na+]i) is critical for various cellular processes.
- The direct impact of glucocorticoids on [Na+]i and cellular transport remains incompletely understood.
Purpose of the Study:
- To investigate the direct effects of glucocorticoids on intracellular sodium levels.
- To elucidate the cellular transport mechanisms involved in glucocorticoid-mediated sodium changes.
- To determine the role of genomic and non-genomic pathways in these effects.
Main Methods:
- Human lymphocytes were utilized to measure cytosolic free sodium concentration ([Na+]i).
- The sodium-sensitive fluorescent dye sodium-binding benzofuran-isophthalate (SBFI) was employed for [Na+]i quantification.
- Dexamethasone was administered, and its effects were assessed in the presence and absence of extracellular sodium, and with specific inhibitors.
Main Results:
- Dexamethasone administration significantly increased lymphocytic [Na+]i.
- This increase was dependent on extracellular sodium and was inhibited by mifepristone and actinomycin D.
- The dexamethasone-induced [Na+]i elevation persisted even after inhibiting the Na+,K(+)-ATPase pump with ouabain.
Conclusions:
- Dexamethasone induces a rapid increase in intracellular sodium concentration in human lymphocytes.
- This effect is likely mediated by a trans-plasma membrane sodium influx.
- Early genomic effects of dexamethasone are implicated in regulating sodium transport systems.
Abstract:
We evaluated the direct effects of glucocorticoids on intracellular sodium content and cellular transport systems. Cytosolic free sodium concentration ([Na+]i) was measured in intact human lymphocytes using the sodium-sensitive fluorescent dye sodium-binding benzofuran-isophthalate. Administration of dexamethasone for 60 min increased lymphocytic [Na+]i from 17.6 +/- 2.0 mmol/L to 24.3 +/- 3.9 nmol/L (n = 12; P < 0.01). The dexamethasone-induced [Na+]i increase was abolished in the absence of extracellular sodium, by mifepristone and by actinomycin D. The dexamethasone-induced [Na+]i increase was also seen after inhibition of Na+,K(+)-ATPase by 1 mmol/L ouabain. The present results indicate that dexamethasone produces a trans-plasma membrane sodium influx probably by early occurring genomic effects.
