Factors controlling adrenal weight and corticosterone secretion in male rats as revealed by median eminence lesions and pharmacological alteration of prolactin secretion

Abstract

To determine whether or not prolactin, as well as ACTH, was involved in the control of adrenal weight and steroid release, lesions in the median eminence which had previoulsy resulted in impaired steroid release and atrophy of the adrenal were placed in animals in which the plasma prolactin was allowed to rise as a result of the lesions or prevented from rising by the administration of the dopamine agonist, CB-154. As previously reported, as the severity of diabetes insipidus (DI) increased as a result of interruption of the supraoptico-hypophyseal tract, adrenal weight declined reaching a nadir at water intakes of approximately 100–150 ml/day. This was followed by a reversal of this trend and an increase in adrenal weight as water intakes increased further. These effects were not modified by CB-154 which was effective to lower the elevated prolactin levels in the animals. In general, adrenal weight correlated with levels of plasma corticosterone and progesterone. The ability of the animals to undergo compensatory adrenal hypertrophy was also impaired by median eminence lesions in the presence or absence of CB-154. Exceptional animals were encountered in which adrenal weight was high and yet plasma corticosterone was low. Treatment of hypophysectomized animals with long-acting ACTH plus maintenance doses of triiodothyronine prevented the adrenal atrophy characteristic of the hypophysectomized animal, thus confirming that ACTH is the most important hormone in the control of adrenal weight. Some role for prolactin is suggested by the fact that elevation of prolactin via the drinking of sulpiride, a dopamine receptor blocker, was associated with a relatively small elevation of adrenal weight and plasma corticosterone. In the animals with lesions, blockade of adrenal function was always found in animals with complete lesions of the median eminence and was usually found if the lesion destroyed the anterior median eminence and extended caudally to the separation of the pituitary stalk. Lesions of the paraventricular nucleus did not block adrenal function, presumably because sufficient CRF neurons were located outside this structure to maintain adrenal function and/or because of the maintenance of considerable vasopressin secretion. Defective adrenal function was usually associated with DI indicative of interruption of the supraoptico-hypophyseal tract and deficient vasopressin secretion; however, several animals were found which had relatively high degrees of DI and yet adrenal function was relatively normal suggesting that CRF is more important than vasopressin in the control of ACTH secretion. Since some animals had relatively normal adrenal function and weight in the presence of severe damage to the median eminence it is possible that other pituitary factors, the release of which would be increased by such lesions, such as α-MSH, may play a role in maintenance of adrenal weight. The possible participation of neural factors also cannot be ruled out.