Effects of corticosteroids on parameters related to Na+ transport by amphibian renal distal cells (A6) in culture.
The present study addresses the effects of the hormones aldosterone and corticosterone, as well as those of dexamethasone, on cultured renal amphibian cells, focusing on parameters thought relevant for the further understanding of the regulation by these steroids of Na+ reabsorption along the renal tubule. Exposure to these steroids of A6 cell monolayers grown on a permeable support produced a motor, dose-dependent, increase in Na+ transport, reflected by the short-circuit current, Isc. (Na+ + K+)-ATPase activity and ouabain binding, both of which are linearly correlated with Isc in control tissue, also increased significantly after steroid treatment. Dexamethasone was consistently more active than corticosterone and aldosterone on the parameters studied. The increase in Isc and (Na+ + K+)-ATPase activity elicited by dexamethasone could be blocked by the glucocorticoid antagonist RU 486, whereas it was only slightly reduced by the mineralocorticoid antagonist, spironolactone. In contrast, the latter strikingly reduced the effects of aldosterone on these parameters, unlike RU 486. Furthermore, the effects of large doses of dexamethasone and aldosterone combined were not additive. Taken together, the data presented appear compatible with the view that the effects of aldosterone on Na+ transport by A6 cells are mediated by a fraction of the receptors involved in the response to dexamethasone; they furthermore raise the question of whether, in lower vertebrates, it is relevant to make a distinction between "gluco" and "mineralo"corticoids.
Lyoussi
B
B
Departement de Physiologie, Université Catholique de Louvain, Bruxelles, Belgium.
Crabbé
J
J
D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000450:Aldosterone / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002460:Cell Line; D003345:Corticosterone / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004594:Electrophysiology; D004848:Epithelium / Q000502:physiology; D005938:Glucocorticoids / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D007686:Kidney Tubules, Distal / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D015735:Mifepristone / Q000494:pharmacology; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D010042:Ouabain / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013148:Spironolactone / Q000494:pharmacology; D014982:Xenopus laevis
D000305:Adrenal Cortex Hormones; D005938:Glucocorticoids; D006727:Hormone Antagonists; D000451:Mineralocorticoid Receptor Antagonists; D011965:Receptors, Glucocorticoid; D013148:Spironolactone; D015735:Mifepristone; D000450:Aldosterone; D010042:Ouabain; D003907:Dexamethasone; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D003345:Corticosterone