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Chronic depression symptoms desensitize renin activity to protect against volume-loading hypertension in Blacks: The SABPA study.

Physiol. Behav.2018 Oct 01;194:474-480. Epub 2018 Jun 28
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摘要


BACKGROUND:Low-renin levels in Blacks have been associated with volume-loading hypertension (HT). Depression symptoms, frequently co-occurring with vascular dysregulation, might reflect a disturbed renin-angiotensin-aldosterone-system (RAAS). We aimed to assess prospective changes (∆) in depression symptoms, RAAS (renin, aldosterone), diastolic blood pressure (DBP), and estimated glomerular filtration rate (eGFR) in a bi-ethnic sex cohort. METHODS:We included 195 Black and White teachers (43.7 ± 9 years) from a South African 3-year prospective study. Hypertension medication users, diabetics and human immunodeficiency virus infected individuals were excluded. Depression symptoms (Patient-Health-Questionnaire-9/PHQ-9), 24 h blood pressure measurements and fasting blood samples were obtained. RESULTS:Blacks had lower renin but higher DBP and eGFR levels at baseline (p ≤ .01) when compared to Whites. Blacks and Whites with depression (PHQ-9 ≥ 10) at baseline developed co-morbidity for having both depression plus DBP-HT at follow-up (Blacks, 49.1%; Whites, 13.1%). At 3-year follow-up, chronic depression symptoms were related to chronic lower renin in Blacks [Adjusted R2 0.20; β -0.37 (-0.66, -0.08), p = .02]. Chronic depression symptoms also predicted DBP hypertension in Blacks [ROC AUC = 0.61 (0.48-0.75); sensitivity/specificity 78.1/46.3%]. No prospective associations existed between depression symptoms, aldosterone and eGFR. CONCLUSION:Chronic depression symptoms in Blacks activated the RAAS system activity with apparent desensitization of renin activity. Chronic depression could be causal to hypertension and in turn, lowers renin activity as a protective mechanism against volume-loading. These findings emphasize the potential impact of depression on the low renin-hypertension phenotype in Blacks in terms of diagnosis and treatment. Copyright © 2018 Elsevier Inc. All rights reserved.

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