Regulation of the seasonal cycle of β-endorphin and ACTH secretion into the peripheral blood of rams
Authors: Ssewannyana E. , Lincoln G. A. , Linton E. A. , Lowry P. J. 
Published: December 2008

ABSTRACT
In a group of 12 adult Soay rams living outdoors near Edinburgh there was a conspicuous seasonal cycle in the peripheral plasma concentrations of β-endorphin, ACTH and cortisol. The concentration of all three hormones increased 5- to 20-fold from winter to summer; the seasonal maximum occurring from May to July for ACTH and cortisol and in August for β-endorphin. At the peak of the cycle the ratio of β-endorphin to N-acetyl-β-endorphin was 22:1. The regulation of the seasonal cycle was investigated in a series of five experiments involving treatments with arginine vasopressin (AVP), corticotrophin-releasing factor (CRF) and the synthetic glucocorticoid, dexamethasone.
Injection of AVP i.v. induced a dose-dependent increase in the plasma concentration of β-endorphin (AVP doses of 0, 0·07, 0·33 and 1·67 μg/kg). AVP (0·33 μg/kg) and CRF (1·67 μg/kg) given alone or in combination (equimolar doses), induced an increase in the plasma concentrations of β-endorphin and ACTH in spring, summer, autumn and winter, and produced a synergistic response when given together. The responses varied with season and were greatest in summer and autumn at the time of the seasonal increase in endogenous secretion. Dexamethasone injected i.v. at 68·04 μg/kg produced a decrease in the plasma concentrations of β-endorphin and ACTH, and the responses were also greatest in summer and autumn. A similar treatment with dexamethasone blocked the AVP-induced increase in the plasma levels of β-endorphin, indicating an action of dexamethasone on the pituitary gland. Administration of ACTH (0·33 μg/kg; i.v.) to rams pretreated with dexamethasone stimulated an increase in the plasma concentration of cortisol; this response varied with season, being greatest in spring at the time of the peak in the seasonal cycle in cortisol secretion. The administration of β-endorphin (0·33 pg/kg) failed to induce an increase in the plasma levels of cortisol at any season. Analysis of the hormone profiles in the control rams based on blood samples collected every 10 min for 8 h revealed pulsatile variations in the plasma concentration of ACTH; some of the spontaneous ACTH peaks were correlated with β-endorphin peaks.
From these results in the Soay ram, we conclude that β-endorphin and ACTH are co-secreted from the pituitary gland following stimulation by AVP and CRF, and that adrenal glucocorticoids stimulated by ACTH can act in a negative feedback role at the level of the pituitary gland to inhibit the release of both β-endorphin and ACTH. These acute studies indicate a parallel control of β-endorphin and ACTH at all stages of the seasonal cycle, and a seasonal change in the secretion of AVP and CRF from the hypothalamus may constitute the 'drive' to the seasonal cycle in both β-endorphin and ACTH. There was, however, a notable difference in the timing of the seasonal cycle in β-endorphin compared with that of ACTH, which indicates some form of differential control of these two pituitary hormones.
Journal of Endocrinology (1990) 124, 443–454