Abstract

SUMMARY l-Thyroxine and 3,5,3′-triiodo-l-thyronine in concentrations of 10−8 m to 10−5 m were shown to increase the oxygen uptake and water transfer down an osmotic gradient in the isolated urinary bladder of Bufo bufo. The increase in water transport after treatment with thyroxine and triiodothyronine was related linearly to the log dose. The increase in O2 uptake and water movement in equimolar concentrations of thyroxine and triiodothyronine were similar but the responses to the latter were more rapid. Substitution of sodium ions by choline in the incubation medium resulted in a fall of oxygen uptake by the bladder, and a slight lowering of water loss. When thyroxine was added, oxygen uptake increased to the same extent in both media but only in sodium saline did water loss increase greatly. Specific enzyme inhibitors prevented the thyroxine-induced increase in water loss across the isolated toad bladder, indicating that metabolic energy is necessary for this alteration in permeability. Triiodothyronine and thyroxine caused an increased water loss across the isolated toad bladder when placed on either the mucosal or serosal surface. Two analogues of the thyroid hormones, 3,5,3′-triiodothyroacetic acid and 3,5,3′,5-tetraiodothyroacetic acid, caused an extremely rapid, but transient, movement of water across the bladder; their action and that of triiodothyronine and thyroxine is compared. An hypothesis is proposed tentatively to account for the mode of action of thyroxine on the permeability of the isolated toad bladder, taking into account the close relationship between increases in water permeability and metabolism, particularly that involving sodium transport.

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