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Am J Physiol Renal Physiol 253: F945-F951, 1987;
0363-6127/87 $5.00
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AJP - Renal Physiology, Vol 253, Issue 5 945-F951, Copyright © 1987 by American Physiological Society

ARTICLES

Na+-H+ exchanger in proximal cells isolated from kidney. II. Short-term regulation by glucocorticoids

M. Bidet, J. Merot, M. Tauc and P. Poujeol
Institut National de la Sante et de la Recherche Medicale, Unite 246, Centre d'Etudes Nucleaires de Saclay, Gif-Sur-Yvette, France.

The purpose of this study was to investigate the acute regulation by glucocorticoid of the Na+-H+ exchanger in isolated renal proximal cells of the rabbit. The changes of intracellular pH (pHi) were determined in a bicarbonate-free buffer by the use of a fluorescent pH probe that may be trapped intracellularly, 2,7-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF). The activity of the Na+-H+ exchanger was estimated by measuring the Na+-induced H+ efflux in BCECF-loaded cells acid loaded with nigericin in choline medium. The uptake of 1.5 mM 22Na was also studied in Na+-depleted cells. Acute application of dexamethasone (1 h at 37 degrees C) increased the activity of the Na+-H+ exchanger. Evidence for this was the fact that the hormone enhanced the rate of Na+-dependent H+ efflux in acid-loaded cells and increased the Na entry in normal pH, sodium-depleted cells. These actions were blocked by 0.5 mM amiloride and were specific to glucocorticoids, since mineralocorticoids (aldosterone) did not promote modification either of the H+ efflux or the Na influx. The effect on the kinetics of amiloride-sensitive Na+-H+ exchange indicated that dexamethasone (DEX) increased the activity by increasing the Vmax of the carrier for external sodium (Vmax control = 26.5 +/- 1.7, DEX = 33.0 +/- 2.4 mmol H+.1-1.min-1, n = 5, P less than 0.001) and for external H+ (Vmax control = 20.6, DEX = 25.8 mmol H+.1-1.min-1, n = 2).(ABSTRACT TRUNCATED AT 250 WORDS)


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