Female rats were subjected to 8 h of daily immobilization for 1, 3, 6, 10 or 15 days. Exposure for 3 days inhibited b.w. and induced adrenal enlargement as well as thymus involution; 6 days of stress elicited atrophy of the ovaries and hypophysis. During the later stages of the experiment, the animals showed a positive metabolic balance, and the initial weight alterations of the endocrine glands either tended to regress or were stabilized. On the 6th day, plasma corticosterone reached a peak which was maintained until the end of the experiment, whereas growth hormone (GH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) titers, as determined by radioimmunoassay, fell to 28, 39 and 55% of control values, respectively, following the 1st period of restraint; prolactin (Prl) decreased by 30% after the 3rd day. Thereafter, the plasma concentrations of these hormones remained low, around 40–60% of control levels, although FSH on The 6th day revealed a transient but significant elevation to 180% of initial values. After 15 days of 6-h-daily immobilization, an injection of LH-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) induced dramatic increases of LH, FSH, Prl and thyrotropin stimulating hormone (TSH) in plasma. On the basis of the morphologic and hormonal changes, it appears that, in agreement with the concept of a shift in adenohypophyseal activity during severe chronic stress, repeated long-term restraint elicits an inverse relationship between the secretion of ACTH and that of GH, LH, Prl and, to a lesser degree, FSH. Such modifications do not seem to be associated with an inability of the pituitary to secrete these hormones, since it is still responsive to releasing factors.
Plasma modifications of adenohypophyseal hormones were investigated in groups of female and male rats stressed for 15, 30 min, 1, 2, 4 or 6 h, either by cold (4°C), forced muscular exercise (FME), or immobilization. GH levels in both female and male rats were consistently decreased by the 3 stressing agents. Immobilization in the female and the 3 stressors in the male elicited an early secretory response of prolactin (Prl), while only in immobilized female rats plasma LH levels showed an early, short-lived increment. A more prolonged exposure to stress had an inhibitory influence on plasma Prl and LH levels in both sexes. FSH concentrations were not modified in females, but were decreased in male rats submitted to either one of the 3 stressors. In both male and female rats plasma TSH levels rose during cold exposure, while they were decreased by FME and by immobilization. Our data indicate that the character of the hormonal secretory response during stress is nonspecific. Indeed, to the exception of the specific stimulation of TSH release by cold, stress-induced hormonal changes are not related to the nature but rather to the intensity and duration of the stressing agent.
To delineate the pattern of adenohypophyseal hormone secretion following chronic stress, adult male rats were exposed daily to 6 h of cold, forced exercise or immobilization for 3, 6, 10, 15, 28 or 42 consecutive days. Groups of these animals were sacrificed at the end of the last stress sessions, and plasma growth hormone (GH), luteinizing hormone (LH), prolactin (Prl) and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay (RIA). Irrespective of the different stimuli used, long-term stress induced a morphologic and hormonal response characterized by decreased ponderal growth, adrenal enlargement, thymus involution and significant diminutions in GH, Prl and LH levels with no modifications in FSH titers. The magnitude and duration of these changes varied with the severity of the stressors.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.