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- W2078791458 abstract "The main purpose of this study is to elucidate the effect of adrenocorticoids on Mg2+-HCO3(-)-ATPase and carbonic anhydrase which are thought to be related to anion transport in mammalian intestinal mucosa and renal tubulus. Rat duodenal mucosa, large intestinal mucosa and kidney cortex were excised and homogenized with mannitol-Tris buffer (pH 7.1) and brush border fraction and cytosol were obtained by a differential fractionation procedure. Brush border Mg2+-HCO3(-)-ATPase and cytosol carbonic anhydrase activities in the duodenal mucosa decreased to 70% and 37% of normal values, respectively 5-11 days after adrenalectomy. Adrenalectomy also decreased significantly both enzyme activities in large intestinal mucosa; on the other hand, renal enzyme activities did not change. Four hours after a single injection of 20-80 micrograms/kg of aldosterone, ip, to adrenalectomized rats, Mg2+-HCO3(-)-ATPase and carbonic anhydrase activities in duodenal mucosa increased gradually to normal or near normal in dose-dependent fashion. Both enzyme activities in large intestinal mucosa were also increased by a larger dose of aldosterone. Again, renal enzyme activities were not affected by any dose of aldosterone. In contrast, corticosterone (1 mg and 4 mg/kg) and dexamethasone (50 micrograms 200 micrograms/kg) had no replacement effect on enzyme activities in all organs. These results showed that the mineralocorticoid, but not glucocorticoids, is a regulator of the enzyme activity of Mg2+-HCO3(-)-ATPase and carbonic anhydrase from intestinal mucosa. The true mechanisms by which both enzymes are activated by aldosterone are not clear at present." @default.
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- W2078791458 date "1989-07-01" @default.
- W2078791458 modified "2023-10-14" @default.
- W2078791458 title "Further studies on the effect of aldosterone on Mg2+-HCO3−-ATPase and carbonic anhydrase from rat intestinal mucosa" @default.
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- W2078791458 doi "https://doi.org/10.1016/0022-4731(89)90362-2" @default.
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- W2078791458 hasPublicationYear "1989" @default.
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