4.3 Article

Determinants and Mechanisms of the Renin-Aldosterone Stress Response

Journal

PSYCHOSOMATIC MEDICINE
Volume 84, Issue 1, Pages 50-63

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PSY.0000000000001018

Keywords

acute psychosocial stress; renin-angiotensin-aldosterone system; adrenocorticotropic hormone; norepinephrine; anticipatory cognitive stress appraisal; Primary Appraisal Secondary Appraisal; ACE = angiotensin-converting enzyme; ACTH = adrenocorticotropic hormone; ANG-I = angiotensin I; ANG-II = angiotensin II; BMI = body mass index; BP = blood pressure; CV = coefficient of variance; CVD = cardiovascular disease; ELISA = enzyme-linked immunosorbent assay; EP = epinephrine; GLM = general linear model; HPA = hypothalamic-pituitary-adrenal; MAP = mean arterial pressure; MDBF = Multidimentional Mood State Questionnaire; MI = maximum increase; NEP = norepinephrine; PASA = Primary Appraisal Secondary Appraisal; PRA = plasma renin activity; RAAS = renin-angiotensin-aldosterone system; SAM = sympathetic-adrenomedullary; SEM = standard error of the mean; VAS = visual analog scale; TSST = Trier Social Stress Test

Funding

  1. German Research Foundation under Germany's ExcellenceStrategy [EXC 2117-422037984]
  2. German Research Foundation [INST 38/550-1]
  3. Swiss National Science Foundation [PP00P1_128565/1]
  4. Stoll VITA foundation
  5. German Scholars Organization [GSO/CZS 2]

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Acute psychosocial stress can activate the renin-angiotensin-aldosterone system, and cognitive stress appraisal processes seem to modulate this stress reactivity.
Objective The renin-angiotensin-aldosterone system (RAAS) plays a relevant role in regulating blood pressure and thus maintaining cardiovascular homeostasis. Although it was recently shown that RAAS parameters are responsive to acute psychosocial stress, the psychobiological determinants of the acute stress-induced RAAS activation have not yet been investigated. In a randomized placebo-controlled design, we investigated potential psychological and physiological determinants of the RAAS response and underlying mechanisms. Methods Fifty-seven young healthy male participants underwent either an acute standardized psychosocial stress test or a nonstress placebo task. We measured aldosterone in plasma and saliva, as well as renin, and the stress-reactive endocrine measures adrenocorticotropic hormone (ACTH), epinephrine, and norepinephrine in plasma at rest, immediately after the task and several times up to 3 hours thereafter. Moreover, we assessed stress-reactive psychological (anticipatory cognitive stress appraisal, mood, physical discomfort) and basal demographic-physiological measures (age, body mass index, blood pressure). Results Acute psychosocial stress elicited changes in all assessed endocrine (p values <= .028, eta(2)(p) values >= 0.07) and stress-reactive psychological measures (p values <= .003, eta(2)(p) values >= 0.15). The basal parameter body mass index, the stress-reactive endocrine parameters ACTH and norepinephrine, and the psychological parameter anticipatory stress appraisal were identified as determinants of higher RAAS parameter reactivity to acute psychosocial stress. The association between anticipatory cognitive stress appraisal and plasma RAAS measures was fully mediated by ACTH increases (p values <= .044, eta(2)(p) values >= 0.05). Conclusions Cognitive stress appraisal processes seem to modulate RAAS stress reactivity. This points to potential clinical implications for psychoeducative therapeutical interventions targeting stress appraisal processes to reduce endocrine stress reactivity.

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