Adrenomedullary function in depressed patients☆
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Cited by (22)
The Neurobiology of Mixed States
2020, Psychiatric Clinics of North AmericaCitation Excerpt :Dopaminergic activation in the ventral tegmental area, substantia nigra, and dorsal raphe nuclei increases wake states and motivational arousal toward salient stimuli.62 Similarly, monoamine hyperactivity also has been related to behavioral symptoms of hyperarousal, such as irritability,63 agitation,20,33 and insomnia.64 Such symptoms have been considered as the core features of both mixed depressives and mixed manic states,1 therefore suggesting that hyperactivation and hyperarousal represent common driving characteristics of both mixed mania and mixed depression.
Immunohistochemistry of catecholamines in the hypothalamic-pituitary-adrenal system with special regard to fatal hypothermia and hyperthermia
2010, Legal MedicineCitation Excerpt :Nad- and DA-immunopositivity in the adrenal medulla may be used as markers to investigate the magnitude of physical stress responses involving the S/A system in death process due to hypothermia and hyperthermia. In fatal intoxication cases, however, adrenomedullary Nad-immunopositivity was relatively higher despite death being mostly preceded by physical inactivity, suggesting a toxic effect on the S/A system [29]. However, the hypothalamus presented different findings involving a lower neuronal DA-immunopositivity in hyperthermia cases, which showed elevated serum and CSF catecholamine levels.
High impact of depression in heart failure: Early diagnosis and treatment options
2008, International Journal of CardiologyCitation Excerpt :In depression, sympathetic nervous system (SNS) hyperactivity is associated with overstimulation of the hypothalamic–pituitary–adrenal (HPA) axis. Likewise, depressed patients frequently show hypercortisolemia and adrenomedullary dysfunction in corticotropic hormone-releasing factor challenge and cortisol non-suppression upon dexamethasone test [2,35,36]. In view of the similarities of these neurohormonal alterations with CHF, depression could facilitate the evolution or progression of CHF via hyperactivity of the SNS or the HPA axis [2].
Mood disorders in the medically ill: Scientific review and recommendations
2005, Biological PsychiatryCitation Excerpt :Depression is linked to increased platelet activation and hypercoagulability (Kop et al 2002; Kuijpers et al 2002; Laghrissi-Thode et al 1997; Lederbogen et al 2001; Musselman et al 1996, 2002; von Känel et al 2001). Evidence suggests depression-related alterations in neurohormonal mechanisms, such as hypothalamic-pituitary-adrenal (HPA) axis hyperactivity and increases in plasma cortisol (Ehlert et al 2001; Maas et al 1994; Plotsky et al 1998), might correlate with increased CHF risk (Francis et al 1993; Pepper and Lee 1999). Behavioral factors also increase risk for cardiac disease for patients with depression who might not adhere to smoking cessation goals, dietary changes, daily aspirin therapy, antihypertensive regimens, or cardiac rehabilitation (Anda et al 1990; Blumenthal et al 1982; Carney et al 1995; Glazer et al 2002; Wang et al 2002).
Why is depression bad for the failing heart? A review of the mechanistic relationship between depression and heart failure
2004, Journal of Cardiac FailureCitation Excerpt :Studies have consistently documented hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis in depressed patients, as reflected by hypercortisolemia, elevated corticotropin-releasing factor in cerebrospinal fluid, decreased adrenocorticotropic hormone response to corticotropin-releasing factor challenge, nonsuppression of cortisol secretion in response to dexamethasone, and pituitary and adrenal gland enlargement (see review36–39). HPA hyperactivity in turn augments sympathetic hyperactivity via central regulatory pathways; this phenomenon has been demonstrated in depressed patients, manifest by elevated plasma norepinephrine as well as a hypersecretory catecholamine response to orthostatic challenge.40,41 However, not all studies have found this association; a report by Carney et al suggested no relationship between norepinephrine levels and depression in a study of 89 patients with CAD (norepinephrine levels for depressed versus nondepressed patients: 280 pg/mL versus 323 pg/mL, values log10 transformed, P = .36).42
Depression and cardiovascular disease: Mechanisms of interaction
2003, Biological PsychiatryCitation Excerpt :Studies have consistently documented HPA hyperactivity in depressed patients, as reflected by elevated corticotropin-releasing factor (CRF) in cerebrospinal fluid, decreased adrenocorticotropic hormone (ACTH) response to CRF challenge, nonsuppression of cortisol secretion in response to dexamethasone, hypercortisolemia, and pituitary and adrenal gland enlargement (for review, see Plotsky et al 1998; Arborelius et al 1999; Ehlert et al 2001). Sympathoadrenal hyperactivity has also been demonstrated in depressed patients, manifest by elevated plasma norepinephrine as well as a hypersecretory catecholamine response to orthostatic challenge (Gold et al 2000; Maas et al 1994), although not all studies have found this association (Carney et al 1999). Therefore, HPA and SA hyperactivity may speed the development of CVD and worsen prognosis for patients with underlying CVD.
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This program was carried out with the cooperation and participation of the Collaborative Program Investigators and Institutions: S.H. Koslow (Project Director), S. Secunda (Deputy Project Director), I. Hanin (Consultant), B. Harris (Protocol Monitor), National Institute of Mental Health; M.M. Katz (Co-Chairman) Albert Einstein College of Medicine; J.W. Maas (Co-Chairman), C. Bowden, R. Schulman, The University of Texas Health Science Center at San Antonio; D.E. Redmond, Jr, Yale University School of Medicine; A. Swann, The University of Texas Health Science Center at Houston; J.M. Davis, S. Chang, D. Garver, J. Javaid, Illinois State Psychiatric Institute; R. Casper, Michael Reese Hospital and Medical Center; J. Mendels, D. Brunswick, A. Frazer, A. Ramsey, S. Stern, Philadelphia VA Medical Center; P.E. Stokes, J. Kocsis, Cornell University Medical College; E. Robins, J. Croughan, Washington University School of Medicine; Nancy Berman, Harbor-UCLA Medical Center. The research was supported by grants UO1 MH38084, UO1 MH26977, UO1 MH26979, UO1 MH26978, UO1 MH31921, and UO1 MH36232.