The effects of various steroids on sodium transport across the toad bladder were examined in vitro. Cortisone, alone, had no effect on sodium transport but was an antagonist of aldosterone. Cortisone was shown to bind to the two non-specific binding sites for steroids in the nucleus of the toad bladder epithelial cells when present at a concentration of 10−7m. At higher concentrations it interacted with the mineralocorticoid receptors and displaced aldosterone from these sites. Cortexolone had a weak stimulating effect on sodium transport and also antagonized the effect of aldosterone. Cortexolone, when present in excess, displaced aldosterone from its receptor sites.
Four types of steroid could be differentiated by their interaction with the mineralocorticoid receptor sites and the subsequent biological response: (a) steroids that bind to the receptors and produce the full biological effect on sodium transport; (b) steroids that do not bind and therefore are incapable of producing a response; (c) steroids that bind to the receptor sites, have no effect alone but inhibit the action of aldosterone; (d) steroids that bind to the receptor sites, produce a partial response on sodium transport and subsequently antagonize the action of aldosterone.
Multiple points of attachment are postulated for the steroid—receptor interaction.
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