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AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 6 1176-R1183, Copyright © 1989 by American Physiological Society
ARTICLES |
J. L. Renfro, N. B. Clark, R. E. Metts and M. A. Lynch
Department of Physiology and Neurobiology, University of Connecticut, Storrs 06268.
To examine the effect of glucocorticoids on sulfate transport by the chick (domestic Gallus gallus) renal tubule we dosed 3-wk-old animals with 60 micrograms dexamethasone/100 g body wt at 24 and 6 h before isolation of renal brush-border (BBM) and basolateral membranes (BLM). Dexamethasone treatment significantly reduced Na-dependent sulfate transport by BBM and had no effect in paired membranes on bicarbonate, proton, or electrical gradient-driven sulfate transport. The glucocorticoid treatment had no statistically significant effect on HCO3-SO4 exchange in the BLM. Kinetic analysis of the dexamethasone effect on the Na-SO4 transport process showed that apparent Vmax was significantly decreased to almost one-half that seen in controls (from 676 to 348 pmol.mg protein-1.5 s-1). The Km in control BBM was 0.40 +/- 0.095 mM and was not significantly different in dexamethasone-treated membranes (0.53 +/- 0.094 mM). To determine whether the dexamethasone-induced decrease in Na-SO4 transport by BBM was indirectly caused by stimulation of Na-H exchange and more rapid dissipation of the initial Na gradient used to drive sulfate uptake, we examined the effect of 0.1 mM amiloride on Na-SO4 uptake by BBM. With amiloride present, dexamethasone treatment caused Vmax to significantly drop from 1,102 to 660 pmol.mg protein-1.5 s-1. Amiloride had no statistically significant effect on the Km. The extent to which amiloride increased Na-SO4 transport and blocked 22Na uptake by BBM did not appear to be related to hormone treatment. The data indicate that glucocorticoids may participate in the regulation of sulfate excretion.
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