Thyroid hormone antagonizes an aldosterone-induced protein: a candidate mediator for the late mineralocorticoid response.
In the urinary bladder of the toad Bufo marinus, the basal rate of synthesis of a number of proteins was modulated in a bidirectional way (i.e., induced or repressed) by aldosterone and by triiodothyronine (T3). Each hormone was therefore characterized by a distinct domain of response. When both hormones were added simultaneously, the two domains consistently overlapped at least for one protein, termed AIP-1, or aldosterone-induced protein 1 (Mr approximately 65 kilodaltons, pi = 6.7, as analyzed by two-dimension gel electrophoresis). The physiological role of AIP-1 is unknown, but could be related to the late mineralocorticoid response. In five experiments, T3 (60 nM, 18-hr incubation) consistently repressed AIP-1, while aldosterone-dependent sodium transport (late response) was significantly inhibited, as previously described. The repression of AIP-1 was also observed as early as 6 hr after aldosterone addition. In addition, sodium butyrate (3 mM), which was previously shown to also selectively inhibit the late mineralocorticoid response, was also able to repress AIP-1. Our results suggest that AIP-1 is one of the proteins involved in the mediation of the late mineralocorticoid response.
D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D002024:Bufo marinus; D002087:Butyrates / Q000494:pharmacology; D020148:Butyric Acid; D000451:Mineralocorticoid Receptor Antagonists; D014176:Protein Biosynthesis; D011499:Protein Processing, Post-Translational; D011506:Proteins / Q000235:genetics; D012323:RNA Processing, Post-Transcriptional; D012964:Sodium / Q000378:metabolism; D014284:Triiodothyronine / Q000494:pharmacology*; D001743:Urinary Bladder / Q000187:drug effects / Q000502:physiology*
D002087:Butyrates; D000451:Mineralocorticoid Receptor Antagonists; D011506:Proteins; D014284:Triiodothyronine; D020148:Butyric Acid; D000450:Aldosterone; D012964:Sodium