Effects of thyroid hormones and aldosterone on mineralocorticoid binding sites in the toad bladder

Summary

In the urinary bladder of the toadBufo marinus triiodothyronine selectively inhibits the late effect of aldosterone on Na⁺ transport. We have investigated whether T₃ might mediate its antimineralocorticoid action by controlling: i) the level of aldosterone binding sites in the soluble (cytosolic) pool isolated from tissues treated with T₃ (60nm) for up to 20 hr of incubation; ii) the kinetics of uptake of³H-aldosterone into cytoplasmic and nuclear fractions after 2 or 20 hr of exposure to T₃. The number and the affinity of Type I (high affinity, low capacity) and Type II (low affinity, high capacity) cytosolic binding sites (measured at 0°C) did not vary significantly after 18 hr of exposure to T₃, while aldosterone-dependent Na⁺ transport was significantly inhibited. In addition, T₃ did not modify the kinetics of uptake (90 min) of³H-aldosterone into cytoplasmic and nuclear fractions of toad bladder incubatedin vitro at 25°C. By contrast, aldosterone itself was able to down-regulate its cytosolic and nuclear binding sites after an 18-hr exposure to the steroid hormone (10 or 80nm). T₃ slightly (20%) but significantly potentiated the down regulation of nuclear binding sites. In conclusion, T₃ does not appear to have major effects on the regulation of the aldosterone receptor, which could explain in a simple manner its antimineralocorticoid action.