Abstract
Previous studies have demonstrated that systemic administration of glucocorticoids stimulates proximal tubule acidification in part by increasing Na+/H+ antiporter activity; however, these studies could not exclude the possibility that changes in Na+/H+ antiporter activity were secondary to glucocorticoid-induced hemodynamic changes. The present study examined the effect of dexamethasone on Na+/H+ antiporter activity in quiescent OKP cells. Na+/H+ antiporter activity was assayed as the initial rate of Na+-dependent pH recovery from an acid load. Intracellular pH was measured using the pH-sensitive dye 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Dexamethasone produced a dose- and time-dependent stimulation of Na+/H+ antiporter activity in OKP cells. Dexamethasone produced a 24% stimulation in Na+/H+ antiporter activity at 10-9 M and an ∼40% stimulation of Na+/H+ antiporter activity at both 10-8 and 10-6 M. The effect of 10-6 M dexamethasone was seen within 4 h of incubation and was due to an increase in maximal velocity (Vmax, 3.03 vs. 1.79 pH units/min) with no change in the affinity constant for sodium (KNa, 47.2 vs. 42.0 mM). The stimulatory effect of dexamethasone on Na+/H+ antiporter activity was blocked by cycloheximide and was not observed with 10-8 M aldosterone. These data demonstrate a direct effect of glucocorticoids to stimulate Na+/H+ antiporter activity in OKP cells.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Renal Fluid and Electrolyte Physiology |
| Volume | 264 |
| Issue number | 6 33-6 |
| State | Published - Jun 1993 |
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Keywords
- Acidification
- Dexamethasone
- Sodium/hydrogen exchanger
ASJC Scopus subject areas
- Physiology
Cite this
Glucocorticoids stimulate Na+/H+ antiporter in OKP cells. / Baum, Michel; Cano, Adriana; Alpern, Robert J.
In: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, Vol. 264, No. 6 33-6, 06.1993.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glucocorticoids stimulate Na+/H+ antiporter in OKP cells
AU - Baum, Michel
AU - Cano, Adriana
AU - Alpern, Robert J.
PY - 1993/6
Y1 - 1993/6
N2 - Previous studies have demonstrated that systemic administration of glucocorticoids stimulates proximal tubule acidification in part by increasing Na+/H+ antiporter activity; however, these studies could not exclude the possibility that changes in Na+/H+ antiporter activity were secondary to glucocorticoid-induced hemodynamic changes. The present study examined the effect of dexamethasone on Na+/H+ antiporter activity in quiescent OKP cells. Na+/H+ antiporter activity was assayed as the initial rate of Na+-dependent pH recovery from an acid load. Intracellular pH was measured using the pH-sensitive dye 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Dexamethasone produced a dose- and time-dependent stimulation of Na+/H+ antiporter activity in OKP cells. Dexamethasone produced a 24% stimulation in Na+/H+ antiporter activity at 10-9 M and an ∼40% stimulation of Na+/H+ antiporter activity at both 10-8 and 10-6 M. The effect of 10-6 M dexamethasone was seen within 4 h of incubation and was due to an increase in maximal velocity (Vmax, 3.03 vs. 1.79 pH units/min) with no change in the affinity constant for sodium (KNa, 47.2 vs. 42.0 mM). The stimulatory effect of dexamethasone on Na+/H+ antiporter activity was blocked by cycloheximide and was not observed with 10-8 M aldosterone. These data demonstrate a direct effect of glucocorticoids to stimulate Na+/H+ antiporter activity in OKP cells.
AB - Previous studies have demonstrated that systemic administration of glucocorticoids stimulates proximal tubule acidification in part by increasing Na+/H+ antiporter activity; however, these studies could not exclude the possibility that changes in Na+/H+ antiporter activity were secondary to glucocorticoid-induced hemodynamic changes. The present study examined the effect of dexamethasone on Na+/H+ antiporter activity in quiescent OKP cells. Na+/H+ antiporter activity was assayed as the initial rate of Na+-dependent pH recovery from an acid load. Intracellular pH was measured using the pH-sensitive dye 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Dexamethasone produced a dose- and time-dependent stimulation of Na+/H+ antiporter activity in OKP cells. Dexamethasone produced a 24% stimulation in Na+/H+ antiporter activity at 10-9 M and an ∼40% stimulation of Na+/H+ antiporter activity at both 10-8 and 10-6 M. The effect of 10-6 M dexamethasone was seen within 4 h of incubation and was due to an increase in maximal velocity (Vmax, 3.03 vs. 1.79 pH units/min) with no change in the affinity constant for sodium (KNa, 47.2 vs. 42.0 mM). The stimulatory effect of dexamethasone on Na+/H+ antiporter activity was blocked by cycloheximide and was not observed with 10-8 M aldosterone. These data demonstrate a direct effect of glucocorticoids to stimulate Na+/H+ antiporter activity in OKP cells.
KW - Acidification
KW - Dexamethasone
KW - Sodium/hydrogen exchanger
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UR - http://www.scopus.com/inward/citedby.url?scp=0027287276&partnerID=8YFLogxK
M3 - Article
VL - 264
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
SN - 0363-6135
IS - 6 33-6
ER -