Adrenocorticotropic hormone (ACTH) is an essential element of the hypothalamic-pituitary-adrenal (HPA) axis. The most important physiological promoter of ACTH release is a corticotrophin-releasing hormone (CRH) (Wein, Kavoussi, Novick, Partin, & Peters, 2012). The most significant variable in regulating the activity of the HPA axis is stress (Wein et al., 2012). Backström and Winberg (2013) note that the major source of stress in humans is presented by social interactions. Thus, the authors emphasize the relation between ACTH release and stress levels in the organism.
The normal operating of the HPA axis is necessary for any human’s health. Disorders in the regulation of glucocorticoid are connected with psychological and physiological conditions such as hypertension, post-traumatic disorder, diabetes, or depression (Arnett, Muglia, Laryea, & Muglia, 2015). Therefore, understanding the way in which HPA output is connected with the reaction to environmental stressors will enable the professionals to find the approaches to regulating the problem (Arnett et al., 2015). Hsu et al. (2012) investigate the behavioral patterns of response to stress.
In their research, Hsu et al. (2012) investigate provide evidence of how a single nucleotide polymorphism in the CRH receptor 1 (CRHR1) gene demonstrates behavioral and neuroendocrine stress vulnerability. The authors conclude that CRHR1 single nucleotide polymorphism rs110402 can eliminate neural responses to emotional stimuli and thus provide a potential vulnerability mechanism for the development of major depressive disorders (Hsu et al., 2012).
The rationale for Regulation of ACTH
Since ACTH is a common response to stress, regulation of ACTH is connected with the treatment of stress disorders (Dunlop, Mansson, & Gerardi, 2012). Dunlop et al. (2012) suggest the following treatment methods of ACTH release: oxytocin, neurosteroids, dopamine, glutamate, neurokinin/Substance P, endocannabinoids, and gamma-aminobutyric acid. These medications are aimed at intensifying memory of fear elimination, interrupting reconsolidation and diminishing fear memories, and promoting engagement in psychotherapy by eliminating fear and developing acceptance of experience (Dunlop et al., 2012).
Melmed (2017) suggests several ways of regulation of the HPA axis.
Cytokines
A better understanding of the evolvement and regulation of the HPA axis comes with the knowledge that the leukemia inhibitory factor (LIF) plays a crucial role in these processes (Melmed, 2017). LIF provokes the transcription of proopiomelanocortin neurons. Cytokines can stimulate the release of ACTH by stimulation of hypothalamic secretion (Melmed, 2017).
Oxytocin
Low-dose perfusion of oxytocin reduces the levels of cortisol and ACTH, Oxytocin works through paroxysmal kinesigenic choreoathetosis and connects to arginine vasopressin (AVP) receptors, but it is not as strong as AVP in provoking the release of ACTH (Melme, 2017).
Glucocorticoids
These are the main negative regulators of ACTH. Glucocorticoids create nongenomic outcomes that occur faster than genomic ones. Glucocorticoids stimulate corticotrophs to inhibit ACTH secretion (Melmed, 2017). A negative response can be described as “long, short, or ultrashort” in accordance with the place and character of the hormone which mediates the response (Melmed, 2017, p. 61). Protracted negative feedback by glucocorticoids performs a significant function by limiting the activation of the HPA axis (Melmed, 2017).
Physiological Regulators of ACTH Secretion
Many physiological issues can impact the ultimate pattern of ACTH release. Such factors include the negative response by glucocorticoids, circadian rhythms, and stress (Melmed, 2017). These aspects influence one another in a combined manner to be able to control the release of ACTH. Also, am important role in the restriction of ACTH release belongs to the immune system, which cooperates with the HPA axis (Melmed, 2017).
References
Arnett, M. G., Muglia, L. M., Laryea, G., & Muglia, L. J. (2015). Genetic approaches to hypothalamic-pituitary-adrenal axis regulation. Neuropsychopharmacology, 41(1), 245-260.
Backström, T., & Winberg, S. (2013). Central corticotropin releasing factor and social stress. Frontiers in Neuroscience, 7, 49-58.
Dunlop, B.W., Mansson, E., & Gerardi, M. (2012). Pharmacological innovations for posttraumatic stress disorder and medication-enhanced psychotherapy. Current Pharmaceutical Design, 18(35), 5645-5658.
Hsu, D. T., Mickey, B. J., Langenecker, S. A., Heitzeg, M. M., Love, T. M., Wang, H.,… Zubieta, J.-K. (2012). Variation in the corticotropin-releasing hormone receptor 1 (CRHR1) gene influences fMRI signal responses during emotional stimulus processing. The Journal of Neuroscience, 32(9), 3253-3260.
Melmed, S. (Ed.). (2017). The pituitary (4th ed.). London, UK: Academic Press.
Wein, A. J., Kavoussi, L. R., Novick, A. C., Partin, A. W., & Peters, C. (Eds.). (2012). Campbell-Walsh urology (10th ed.). Philadelphia, PA: Elsevier Saunders.