The Renin-Angiotensin-Aldosterone system in patients with depression compared to controls – a sleep endocrine study

Abstract

BackgroundHypercortisolism as a sign of hypothamamus-pituitary-adrenocortical (HPA) axis overactivity and sleep EEG changes are frequently observed in depression. Closely related to the HPA axis is the renin-angiotensin-aldosterone system (RAAS) as 1. adrenocorticotropic hormone (ACTH) is a common stimulus for cortisol and aldosterone, 2. cortisol release is suppressed by mineralocorticoid receptor (MR) agonists 3. angiotensin II (ATII) releases CRH and vasopressin from the hypothalamus. Furthermore renin and aldosterone secretion are synchronized to the rapid eyed movement (REM)-nonREM cycle.MethodsHere we focus on the difference of sleep related activity of the RAAS between depressed patients and healthy controls. We studied the nocturnal plasma concentration of ACTH, cortisol, renin and aldosterone, and sleep EEG in 7 medication free patients with depression (1 male, 6 females, age: (mean +/-SD) 53.3 ± 14.4 yr.) and 7 age matched controls (2 males, 5 females, age: 54.7 ± 19.5 yr.). After one night of accommodation a polysomnography was performed between 23.00 h and 7.00 h. During examination nights blood samples were taken every 20 min between 23.00 h and 7.00 h. Area under the curve (AUC) for the hormones separated for the halves of the night (23.00 h to 3.00 h and 3.00 h to 7.00 h) were used for statistical analysis, with analysis of co variance being performed with age as a covariate.ResultsNo differences in ACTH and renin concentrations were found. For cortisol, a trend to an increase was found in the first half of the night in patients compared to controls (p < 0.06). Aldosterone was largely increased in the first (p < 0.05) and second (p < 0.01) half of the night. Cross correlations between hormone concentrations revealed that in contrast to earlier findings, which included only male subjects, in our primarily female sample, renin and aldosterone secretion were not coupled and no difference between patients and controls could be found, suggesting a gender difference in RAAS regulation. No difference in conventional sleep EEG parameters were found in our sample.ConclusionHyperaldosteronism could be a sensitive marker for depression. Further our findings point to an altered renal mineralocorticoid sensitivity in patients with depression.

Chronic stress impacts the cardiovascular system: animal models and clinical outcomes

“…The activity of the RAAS in a study of 1,743 individuals was higher in depressed people and those who lived alone (129). Some investigators suggest aldosterone as a marker of depression (234). Central activation of mineralocorticoid receptors leads to sympathetic overactivity and increased secretion of proinflammatory cytokines both in central and peripheral tissues (113).…”

Association of CYP11b2 Gene Polymorphism of Aldosteron-Synthase with the Risk of Myocardial Infarction with ST-Segment Elevation

“…В дослі-дженні INTERHEART по виявленню асоційованих з ІМ факторів ризику, що проводилось у 52 странах світу, тривога і депресія займає 3 місце в числі факторів ризику [18]. Murck H., et al 2003, у пацієнтів з депресією, навіть без кардіоваскулярної патології, знайшли підвищення рівня альдостерона та назвали його маркером депресії [13]. В експери-ментальних дослідженнях стрес та дистрес супро-воджувались більш високими рівнями утворення альдостерона [10].…”

Allele and Genotype Frequency of Polymorphous Variants of ATIIR1 and CYP11b2 Genes in Patients with STEMI with the Presence of Anxiety and Depressive Conditions

“…Murck H., et al, 2003, у пацієнтів з депресією, навіть без кардіоваскулярної патології, знайшли підвищення рівня альдостерона та назва-ли його маркером депресії [15]. В експерименталь-них дослідженнях стрес та дистрес супроводжува-лись більш високими рівнями утворення альдосте-рону.…”