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Cellular mechanisms regulating adrenocorticotropin release.
Journal of Receptor Research
|January 1, 1984
Summary
Corticotropin-releasing factor (CRF) and other factors stimulate ACTH release, while glucocorticoids and somatostatin (SRIF) inhibit it. These interactions fine-tune corticotroph activity, crucial for stress response.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Signaling
Background:
- The anterior pituitary gland plays a crucial role in the stress response by releasing adrenocorticotropic hormone (ACTH).
- Understanding the regulation of ACTH release is vital for comprehending physiological responses to stress.
Purpose of the Study:
- To investigate the factors regulating ACTH release from a mouse anterior pituitary tumor cell line (AtT-20/D16-16).
- To elucidate the intracellular mechanisms involved in mediating ACTH secretion and its regulation.
Main Methods:
- Utilized the AtT-20/D16-16 mouse anterior pituitary tumor cell line.
- Investigated the effects of corticotropin-releasing factor (CRF), catecholamines, vasoactive intestinal peptide (VIP), glucocorticoids, and somatostatin (SRIF) on ACTH release.
Main Results:
- CRF, catecholamines, and VIP were found to stimulate ACTH release.
- Glucocorticoids and SRIF inhibited ACTH secretion; glucocorticoids suppressed both synthesis and release.
- SRIF employed multiple mechanisms to inhibit stimulated ACTH release.
- Cyclic AMP and calcium ions (Ca++) function as key second messengers in receptor-mediated ACTH release, with potential involvement of other mediators.
Conclusions:
- A complex interplay exists between stimulatory factors (like CRF) and inhibitory factors (like glucocorticoids and SRIF) in regulating corticotroph activity.
- This fine-tuned regulation of ACTH release is essential for the organism's adaptive response to stress.