PubMed · 4283956
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O Nery, J S de Mello. 1965. [Hypsarrhythmia].. https://pubmed.ncbi.nlm.nih.gov/4283956/
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Corticotropin-releasing hormone (CRH) is the primary hypothalamic releasing factor that mediates the mammalian stress response. The CRH-binding protein (CRH-BP) is secreted from corticotropes, the pituitary CRH target cells, suggesting that the CRH-BP may modulate hypothalamic-pituitary-adrenal (HPA) axis activity by preventing CRH receptor stimulation. Transgenic mice were generated that constitutively express elevated levels of CRH-BP in the anterior pituitary gland. RNA and protein analyses confirmed the elevation of pituitary CRH-BP. Basal plasma concentrations of corticosterone and adrenocorticotropin hormone (ACTH) are unchanged, and a normal pattern of increased corticosterone and ACTH was observed after restraint stress. However, CRH and vasopressin (AVP) mRNA levels in the transgenic mice are increased by 82 and 35%, respectively, to compensate for the excess CRH-BP, consistent with the idea that CRH-BP levels are important for homeostasis. The transgenic mice exhibit increased activity in standard behavioral tests, and an altered circadian pattern of food intake which may be due to transgene expression in the brain. Alterations in CRH and AVP in response to elevated pituitary CRH-BP clearly demonstrate that regulation of CRH-BP is important in the function of the HPA axis.
BACKGROUND: An escape from the dexamethasone-induced suppression of pituitary-adrenocortical activity can be provoked by corticotropin-releasing hormone (CRH) in depressed patients, but not in healthy controls. One important antagonist of the CRH-stimulated secretion of corticotropin (ACTH) and cortisol is atrial natriuretic hormone (ANH). METHODS: To study a potential role of ANH in the dexamethasone-CRH test, we investigated 7 healthy men who did not suppress cortisol below 40 ng/mL after they had received 0.5 mg dexamethasone the evening before. RESULTS: We found 1) that the CRH-stimulated ACTH and cortisol secretion was significantly reduced by the administration of ANH in comparison to saline; and 2) that there was an increased pituitary-adrenocortical ratio. CONCLUSIONS: Our results support the view that ANH may also be involved in the frequently observed nonsuppression after dexamethasone during depression. Biol Psychiatry.
The hypothalamus-pituitary-adrenal axis of the sheep fetus plays a critical role in fetal development, responsiveness to stress, and initiation of parturition. We have recently reported that the fetal lung contains and secretes significant amounts of immunoreactive adrenocorticotropin (iACTH). The present study was designed to identify the molecular weight profile and the cellular location of iACTH in this tissue. iACTH extracted from fetal lung was immunoprecipitated, electrophoresed, and immunoblotted. Pulmonary iACTH was found in several molecular forms. The largest peptides appeared as doublets, and had molecular weights similar to POMC (32, 33 kD). Smaller peptides appeared in molecular weights (17, 24, and 27 kD) which were not consistent with the post-translational processing of POMC in fetal pituitary, but which were consistent with known processing of POMC by chromaffin granule aspartyl protease. None of the molecular forms of iACTH were glycosylated. Immunohistochemistry revealed that the iACTH was contained within bronchial epithelium and within groups of cells within the parenchyma of the lung. Both of these types of cells are consistent with pulmonary neuroendocrine cells. The distribution of neuroendocrine cells and apparent concordance with the iACTH-positive cells was confirmed by immunostaining for neuron specific enolase, a marker for neuroendocrine cells within the lung. We conclude that the lung contains unprocessed and partially processed POMC within cells known to contain neuropeptides. We speculate that secretion of the POMC-related peptides from these cells is physiologically important in the late-gestation fetus.