Effect of indomethacin in vivo and PGE2 in vitro on MTAL Na-K-ATPase of the rat kidney |
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Authors: | Hanna Wald Pnina Scherzer Dvora Rubinger Mordecai M Popovtzer |
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Institution: | (1) Nephrology and Hypertension Services, Hadassah University Hospital, POB 12000, 91120 Jerusalem, Israel |
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Abstract: | We have previously shown that prostaglandin synthesis inhibition in rats which reduces urinary excretion of PGE2 and sodium, is associated with increased Na-K-ATPase activity in renal medulla. To further characterize this interaction
studies were performed in isolated segments of medullary thick ascending limb of Henle's loop (MTAL) in rats. The effect of
pretreatment with indomethacin in vivo and incubation with PGE2 in vitro on MTAL Na-K-ATPase activity was studied. Pretreatment of rats with indomethacin increased Na-K-ATPase of the MTAL
from 37.2±2.0×10−11 mol/mm/min in controls to 62.7±2.2 (p<0.001) while Mg-ATPase was only slightly decreased. Incubation of MTAL Na-K-ATPase
from indomethacin pretreated rats with increasing concentration of PGE2 in vitro dose dependently inhibited MTAL Na-K-ATPase activity with no effect on Mg-ATPase. Baseline Na-K-ATPase was 62.7±2.2
in MTAL from indomethacin pretreated rats and decreased to 36.9±1.4 (p<0.001) with 1 uM of PGE2, to 26.5±2.3 (p<0.001) with 10 uM PGS2 and to 22.0±1.0 (p<0.001) with 100 uM PGE2. 100 uM PGE2 in the incubation medium inhibited MTAL Na-K-ATPase of intact rats from 37.2±2 to 21.3±1.2 (p<0.001) and completely abolished
the indomethacin induced increase in MTAL Na-K-ATPase. The results of this study show stimulation of MTAL Na-K-ATPase by pretreatment
with indomethacin in vivo and, direct inhibition of MTAL Na-K-ATPase by PGE2 in vitro. These findings suggest that the increase in MTAL Na-K-ATPase induced by pretreatment with indomethacin may stem
directly from PGE2 depletion. These observations are consistent with direct inhibitory effect of PGE2 on Na reabsorption in the MTAL. |
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Keywords: | Na-K-ATPase PGE2 Indomethacin MTAL |
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