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ABSTRACT
The effects of selective agonists and antagonists of type 1 (V1) and type 2 (V2) vasopressin receptors on the secretion of ACTH in vitro by segments of adenohypophysial tissue and in vivo in rats pretreated with pentobarbitone and chlorpromazine were studied in the presence and absence of the 41 amino acid-containing peptide, corticotrophin-releasing factor-41 (CRF-41). The non-selective vasopressin receptor agonist, arginine vasopressin (AVP) and the V1-receptor agonist, felypressin caused dose-related increases in ACTH release in vivo and in vitro but the V2-receptor agonist, desmopressin was only weakly active in this respect. Their actions in vitro were antagonized competitively by the V1-receptor antagonist, d(C2H5)2-AVP, but were unaffected by the V2-receptor antagonist, d(CH2)5-d-Iso2-Thr4-AVP. Arginine vasopressin, felypressin and desmopressins in concentrations considerably lower than those necessary to elicit directly the release of ACTH, potentiated, in a dose-related manner, the activity of CRF-41 in vitro. The potentiating effects were not antagonized by the V2-receptor antagonist or by low concentrations of the V1 -receptor antagonist. At a higher concentration, the V1-receptor antagonist reduced, but did not abolish, the potentiating effects of AVP and its analogues. However, at this concentration, it also exhibited weak intrinsic activity and, like the agonists, potentiated the response to CRF-41. The results suggest that the direct effect of AVP on ACTH release is mediated by V1-like receptors. The vasopressin receptors involved in the potentiation of CRF-41 activity appear to be different.
J. Endocr. (1987) 113, 389–396
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Peripheral leucocytes secrete corticotrophin (ACTH) and other pro-opiomelanocortin (POMC)-derived peptides when challenged with appropriate neurochemical stimuli (Smith, Morrill, Meyer & Blalock, 1986). The immunoreactive corticotrophin (ir-ACTH), which has been identified in human peripheral leucocytes infected virally or treated with endotoxin (Smith & Blalock, 1981) and in mouse spleen macrophages (Lolait, Lim, Toh & Funder, 1984), is indistinguishable chromatographically and immunologically from authentic ACTH (Smith, Meyer & Blalock, 1982; Smith et al. 1986) and exhibits marked steroidogenic activity when injected into hypophysectomized mice (Smith et al. 1982) or incubated with cultured Y-1 adrenal cells (Smith et al. 1986). Moreover, the mechanisms controlling its secretion appear to be similar to those effecting ACTH release from the anterior pituitary gland (Smith et al. 1986). These surprising findings add further support to the novel concept that the interactions between the neuroendocrine and immune systems, which are apparent in a number of physiological and pathological
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ABSTRACT
Administration of pregnant mare serum gonadotrophin (PMSG) to peripubertal rats, aged 27 days, induces ovulation provided the animals weigh more than 60 g at the time of the injection. In an attempt to determine whether the apparent immaturity of the ovaries in smaller rats is associated with an inability of the pituitary gland to secrete LH, the biological and immunological properties of LH in peripubertal PMSG-treated rats were examined. A single injection of PMSG caused a marked hypersecretion of LH in rats aged 27 days. The LH in the plasma of rats weighing more than 60 g was active in both the radioimmunoassay and the cytochemical bioassay but that in smaller rats was active only in the former. Plasma from both groups of rats stimulated the release of testosterone from dispersed Leydig cells.
Luteinizing hormone-releasing hormone stimulated the secretion, in vitro, of immunoreactive, cytochemically active LH by pituitary tissue from rats weighing over 60 g. The LH released in vitro from tissue from the smaller animals, like that in their plasma, was active in the radioimmunoassay but not in the cytochemical system. The results suggest that an abrupt change in the nature of LH occurs at puberty and that ovulatory cycles commence only when the pituitary gland secretes the adult form of LH with a full spectrum of biological activity.
J. Endocr. (1985) 104, 173–177
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Introduction
Communication between the neuroendocrine and immune systems is crucial to host defence in both health and disease for it provides a humoral means whereby the central nervous system may fine tune the immune system and thereby bring to bear the influence of a variety of physical, emotional and environmental factors. In the past decade, several lines of communication between the two systems have been identified. These include direct autonomic innervation of lymphoid tissues and humoral factors derived from immune cells (e.g. cytokines, eicosanoids, peptides) and peripheral endocrine glands (e.g. peptides, steroids). Central to this complex interplay are the thymic hormones, a heterogeneous family of polypeptides produced by the thymic epithelium whose members include thymosin α1, thymosin β4, thymopoietin, thymulin, MB-35 and a number of less well-characterized peptides (Table 1). These peptides possess a spectrum of immunoregulatory properties. In addition, they provide the basis of a significant humoral
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ABSTRACT
Opioid substances have been shown to stimulate and depress the secretion of ACTH in the rat. Their opposing actions appear to be mediated in part by specific receptors in the hypothalamus which influence the secretion of corticotrophin-releasing factor (CRF). In an attempt to determine the physiological role of these receptor systems, experiments were carried out in which the plasma ACTH and serum corticosterone concentrations were determined before and after stress in rats treated s.c. with selective antagonists of μ-(naloxone, naltrexone), δ-(ICI 174864) and κ-(MR2266) opioid receptors. Neither naloxone (25–100 μg/100 g) nor naltrexone (50 μg/100 g) influenced the resting plasma ACTH or serum corticosterone concentrations. However, both inhibited (P < 0·01) the secretion of the two hormones elicited normally by surgical stress (laparotomy under ether anaesthesia). ICI 174864 (30–100 μg/100 g) also had little effect on resting hypothalamo-pituitary-adrenocortical (HPA) activity but, at the highest dose, it caused a small (P < 0·05) potentiation of the response to surgery. In contrast, MR2266 (150–300 μg/100 g) produced marked activation of the HPA system and not only stimulated the resting secretion of ACTH and corticosterone but also potentiated and prolonged the HPA response to stress.
The results suggest that μ- and κ-opioid receptors mediate opposing actions of endogenous opioid peptides, both of which may be physiologically important in the regulation of CRF release.
Journal of Endocrinology (1989) 121, 213–220
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SUMMARY
Pituitary and plasma ACTH and plasma corticosterone were measured at various times after adrenal enucleation or adrenalectomy. The changes in ACTH could be inversely correlated with those in plasma corticosterone. They could also be prevented by maintenance therapy with the steroid. The results indicate that the corticosteroids control both the release and the synthesis of ACTH but that their effect is predominantly on the release of the hormone.
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SUMMARY
The cytochemical assay for ACTH has been adapted into a method for the detection and determination of potential corticotrophin releasing factors. Of the many putative transmitter substances tested, only the posterior pituitary polypeptides resembled hypothalamic extracts in causing dose-related increases in both pituitary ACTH content and release. Vasotocin was the most active of the compounds studied and, unlike the vasopressins, its dose–response relationships closely resembled those of hypothalamic extracts. The increase in ACTH release induced by hypothalamic extract or vasopressin was reduced by corticosterone, cortisol or progesterone but not by testosterone or oestradiol, but the increase in pituitary ACTH content was not affected by any of these steroids.
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SUMMARY
Changes in pituitary and plasma corticotrophin (ACTH), estimated by redox bioassay, were correlated with changes in plasma corticosterone in adrenalectomized rats, with and without corticosterone treatment, before and after exposure to stress. After adrenalectomy, the plasma ACTH concentration was persistently increased. The pituitary ACTH content declined and then increased markedly. These changes were prevented by physiological doses of corticosteroids. Stress caused only a small rise in the plasma ACTH concentration in intact and sham-operated rats but a marked increase in adrenalectomized animals. This exaggerated response was reduced to normal by physiological doses of corticosterone. Prolonged treatment with higher doses of corticosterone was necessary to abolish completely the adrenocorticotrophic response to stress. However, one injection of the steroid, in a dose sufficient to raise the plasma corticosterone concentration to a similar level, did not impair the stress-induced release of ACTH. The results suggest that the synthesis and the basal release of ACTH are directly controlled by the concentration of corticosteroid in the blood, but the corticosteroids exert only a delayed effect in modulating the stress-induced release of the hormone.
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The precise nature of the impairment of hypothalamo-pituitary-adrenocortical (HPA) activity which follows prolonged corticosteroid treatment is not yet understood. To study this problem, hypothalamic corticotrophin releasing hormone (CRH) content, pituitary ACTH content and the functional capacity of adenohypophysial tissue in vitro were measured in rats after treatment with betamethasone. The content of CRH and ACTH in the hypothalamus and pituitary gland respectively were markedly reduced. After stopping the treatment the hormone concentrations in both structures returned to normal with the rise in the hypothalamus preceding that in the pituitary gland. Adenohypophysial tissue from betamethasone-treated rats incubated with hypothalamic extracts from control animals showed a considerable reduction in its ability to synthesize and release ACTH. However, corticotrophin release was impaired in adenohypophyses removed from untreated rats and incubated with betamethasone but synthesis was not affected. The physiological significance and the possible clinical relevance of the results are discussed.
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ABSTRACT
The influence of various endocrine and environmental factors on pituitary-ovarian function was studied in peripubertal rats treated with pregnant mare serum gonadotrophin (PMSG). Pregnant mare serum gonadotrophin induced ovulation in rats aged 27 days provided they weighed over 60 g. The response was preceded by a marked hypersecretion of LH which was detectable by radioimmunological and biological assay methods. In contrast, smaller rats of the same age did not ovulate in response to PMSG apparently because of the secretion of a pleiomorphic form of LH which, although immunoreactive, appeared to be biologically inactive. Ovarian function, assessed by response to exogenous gonadotrophins and by measurement of 125I-labelled human chorionic gonadotrophin binding, was normal despite the presence of the biologically inactive pleiomorph. Exposure of the small PMSG-treated rats to a high environmental temperature (39 °C) or treatment with corticosterone or GH altered the nature of the LH in the blood so that it was active in both assay systems and facilitated ovulation as also did ACTH. The results suggest that the abrupt change in the nature of the LH released by the pituitary gland essential for the initiation of ovulation may be affected by GH, corticosterone or a raised environmental temperature.
J. Endocr. (1985) 104, 179–183
