Thyroidal weights, mean acinar cell heights and the performance of the thyroidal iodide concentrating mechanism were examined in groups of intact, hypophysectomized and hypo-physectomized-thyrotropin (TSH) treated rats maintained on a low I (Remington) diet or a high I (Rockland) regimen for 19-20 days. Although the thyroids and the pituitaries of intact I deficient rats showed no morphological evidence of thyrotropic activation, the thyroid: serum iodide gradients (T/S) were greatly elevated and the capacity of the thyroids for "trapped" iodide was expanded. The low I regimen had no effect on the morphological regression of the thyroids of hypophysectomized rats and the T/S in these animals was also lower than in normal rats, albeit significantly higher than in Rockland diet fed hypophysectomized controls. An effect of I intake on the thyroidal iodide "trap" in the absence of TSH is suggested. I deficiency markedly increased the effectiveness of exogenous TSH on the T/S of hypophysectomized rats, without enhancing the influence of the hormone on thyroid morphology. A comparison is made with previously encountered similar effects of propylthiouracil treatment and the mechanisms possibly involved are discussed. It is concluded that elevated thyroidal I uptake may precede other changes of the pituitary-thyroid axis in I deficient states, owing to an augmented response of the thyroidal iodide "trap" to TSH.