Pinocytosis persists in the ileum of hypophysectomized rats unless closure is induced by thyroxine or cortisone.

It was previously reported that in rats hypophysectomized at 6 days of age, the apicotubular system that permits the entrance of macromolecules closes spontaneously in the duodenal epithelium. Extending these observations to the ileum, where pinocytosis is nutritionally important in the suckling rat, now reveals that in the absence of the hypophysis, closure of the surface does not occur. Hence, the failure of growth that sets in during the fourth postnatal week appears not to be due to malnutrition consequent on the cessation of intracellular digestion. Treatment of the hypophyseoprivic sucklings with either thyroxine or cortisone from 15 to 23 days causes the disappearance of the apical infoldings, vesicles, and giant vacuole characteristic of the suckling stage. Instead, the cells exhibit all of the ultrastructural features typical of mature ileal epithelium. The effects of the two hormones differed in that cortisone caused a slightly greater lengthening of the microvilli. These results further extend the evidence indicating that either thyroid hormone or glucocorticoid can activate the complete regulatory program that brings about the redifferentiation of the intestinal epithelium from the suckling to the mature type.     

ACTH and corticosterone response to naloxone and morphine in normal, hypophysectomized and dexamethasone-treated rats

The effect of opiate receptors blocker naloxone on ACTH and corticosterone secretion in normal, dexamethasone-treated and hypophysectomized rats was studied. A dose-related increase in plasma corticosterone level was found at 45 min after s.c. injection of naloxone in a dose range of 0.25-2.0 mg kg-1. The rise in plasma corticosterone was preceded by a slight increase in plasma ACTH. Acute morphine administration in a relatively low dose (6 mg kg-1 s.c.) induced a significant rise in both plasma ACTH and corticosterone levels. Dexamethasone treatment was followed by low basal corticosterone level, by total inhibition of the stress response and response to morphine injection, while the response to ACTH administration was normal. Under these circumstances as well as in rats 6 days after hypophysectomy, naloxone failed to increase plasma corticosterone levels. It is concluded that a direct stimulation of corticosteroid biosynthesis in adrenal cortex is not involved in the mechanism of naloxone-induced activation of pituitary-adrenocortical function.