STRUCTURE AND FUNCTION OF INTRAOCULAR HYPOPHYSEAL GRAFTS IN THE HYPOPHYSECTOMIZED MALE RAT12

Abstract

IT IS becoming increasingly probable that the classical “feed-back” or “servo” theory of target gland-pituitary interplay does not adequately describe the actual glandular interrelations. For example, studies of various metabolic stimulants and pyrogenic agents show that the level of plasma protein bound iodine (PBI) does not necessarily regulate output of thyroidstimulating hormone (TSH) by the pituitary (1). Such output can be suppressed even in rats synthesizing no thyroid hormone so long as a normal or high metabolic rate is maintained (1). The results of these studies suggest that not the actual level of circulating thyroid hormone, but one (or more) of its metabolic effects acting directly or indirectly through the central nervous system is (or are) the crucial element (s) in the regulation of pituitary output of TSH. If the determining substance(s) act directly on the pituitary beta cells (source of TSH), the actual anatomical location of these cells, assuming adequate vascularization, should not be of great importance.