232 /. /. Christian 



ine, but rather to one or more of its peripheral metabohc actions (Goldberg 

 et al., 1957) . The secretion of thyrotropin from the pituitary is undoubtedly 

 under the control of the hypothalamus (D'Angelo and Traum, 1958; 

 Harris and Woods, 1958, Harris, 1959). Like the secretion of adrenocorti- 

 cotropin, the secretion of thyrotropin appears to be controlled by a humoral 

 factor from the hypothalamus (Brown-Grant et al., 1957). Section of the 

 pituitary stalk leads to a loss of the inhibitory response of the thyroid to 

 restraint or pain, and regeneration of the pituitary portal vessels is accom- 

 panied by a return of this response (Harris, 1955a, b; Reiclilin, 1957a, b). 

 The thyroid remains at least partially responsive to exogenous TSH when 

 the pituitary stalk is sectioned (Reichlin, 1957a, b; Harris and Woods, 

 1958). There is also evidence that the hypothalamus is necessary for a 

 decreased blood concentration of thyroid hormone to effect an increased 

 secretion of TSH (Greer, 1951; 1952; Bogdanove and Halmi, 1953; Harris 

 and Woods, 1958; D'Angelo and Traum, 1958). Increased activity of the 

 thyroid accompanies electrical stimulation of the anterior portion of the 

 median eminence, but not other parts of the hypothalamus (Harris and 

 Woods, 1958). The hypothalamic factor responsible for stimulating the 

 release of TSH does not appear to be contained in or associated with 

 Pitressin (Reichlin, 1957a; D'Angelo and Traum, 1958), but little else is 

 known of the nature of this factor. In addition to these regulating factors, 

 the release of TSH is also affected by cortisone and ACTH (Brown-Grant 

 et al., 1954c) . Cortisone and ACTH inhibit the release of radioiodine from 

 the thyroid of rabbits and rats, probably by inhibiting the release of TSH, 

 although the mechanism by which this is accomplished is unknown (Brown- 

 Grant et al., 1954b, c; Brown-Grant, 1955). Cortisone and ACTH have 

 also been reported to inhibit the uptake of radioiodine by the thyroid of 

 rats (Money et al., 1950; Albert et al., 1952; Perry, 1951; Verzar and Vido- 

 vic, 1952) and of humans (Perry, 1951; Kuhl and Ziff, 1952; Albert et al., 

 1952; Berson and Yalow, 1952). However, reports of decreased uptake of 

 radioiodine must be interpreted with caution, as it may reflect a lowered 

 concentration of circulating iodide as a result of increased renal clearance 

 of iodide following treatment with cortisone or ACTH (Brown-Grant et al., 

 1954c) . Adrenalectomy inhibits the release of iodine and therefore of 

 thyroid hormone from the thyroid glands of rats (Fllickiger and Verzar, 

 1955). Bastenie and Ermans (1958) have shown that cortisone, in addition 

 to its effect on the secretion of TSH, inhibits the stimulating effect of 

 thyroxine on oxygen consumption and phosphorus turnover but fails to 

 inhibit these actions of triiodothyronine. These authors concluded that 

 cortisone inhibits the peripheral degradation of thyroxine to triiodothyro- 

 nine. Nevertheless, there is little doubt that cortisone and ACTH do inhibit 



