Endothelin-1 and Psychosocial Risk Factors for Cardiovascular Disease

Yammine, Luba; Kang, Duck Hee; Baun, Mara M.; Meininger, Janet C.

doi:10.1097/psy.0000000000000026

Cited by 19 publications

(19 citation statements)

References 44 publications

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“…These natriuretic peptides also demonstrate anxiolytic behavior, whereas both animal and human studies suggest that these natriuretic peptides partially suppress the HPA axis (12)(13)(14)(15). C-terminal proendothelin-1 (CT-proET) is a vasoconstrictor produced by endothelial and vascular smooth muscle cells and can increase proinflammatory cytokine levels such as interleukins (interleukin-1 and interleukin-1 receptor antagonist [IL-1Ra]) (16,17). Of these cardiovascular markers, only NT-proBNP has previously been tested for association with psychosocial/socioeconomic status (SES) factors in a population context (18).…”

Section: Introductionmentioning

confidence: 99%

The Predictive Value of Depressive Symptoms for All-Cause Mortality

Hughes

Patterson

Appleton

et al. 2016

Psychosomatic Medicine

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Section: Introductionmentioning

confidence: 99%

The Predictive Value of Depressive Symptoms for All-Cause Mortality

Hughes

Patterson

Appleton

et al. 2016

Psychosomatic Medicine

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“…The multivariable model controlled for factors that have the potential of influencing ET-1 level, i.e. left ventricular ejection fraction [LVEF] [15], hypertension [25], diabetes [26], use of beta-blockers [27] and statins [28], current smoking, age [29], race/ethnicity and gender [30]. Descriptive statistics and multivariable models of ET-1T were examined using SPSS 19 statistical package for Windows (SPSS Inc, Chicago, Illinois).…”

Section: Methodsmentioning

confidence: 99%

Severe depressive symptoms are associated with elevated endothelin-1 in younger patients with acute coronary syndrome

Yammine

Frazier

Padhye

et al. 2014

Journal of Psychosomatic Research

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Objective To explore the relationship of depressive symptom severity to circulating Endothelin (ET) – 1 in younger patients with acute coronary syndrome (ACS). Younger patients report greater depressive symptom severity, which predicts poorer post-ACS prognosis. The pathways linking depression to post-ACS prognosis require further elucidation. ET-1 is a potent endogenous vasoconstrictor which has been previously linked to adverse post-ACS outcomes. Methods The sample (n=153) included males ≤50 years of age and females ≤55 years of age who participated in a larger study. Blood samples for ET-1 assessment were collected within 2–3 hours of ACS admission. Depressive symptoms were assessed with the Beck Depression Inventory (BDI) II within 2–5 days of admission. ET-1 was treated as a transformed continuous variable (ET-1T). BDI-II scores were classified into four categories using conventional thresholds demarcating mild, moderate, and severe levels of depressive symptoms. The relationship of classified BDI-II score to ET-1T was examined in simple and multivariable linear regression models. Results Classified BDI-II score was related to ET-1T in both unadjusted (χ2 = 9.469, p = 0.024) and multivariable (χ2 = 8.430, p = 0.038) models, with ET-1T being significantly higher in patients with severe depressive symptoms than in those with mild and moderate depressive symptoms. Conclusions In this sample of younger post-ACS patients, severe depressive symptoms were associated with elevated ET-1. We acknowledge that the observed association could be eliminated by the inclusion of some unmeasured variable(s). Longitudinal research should examine whether ET-1 mediates the relationship of depressive symptoms to long-term post-ACS outcomes.

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“…More important, prior studies have highlighted the importance of both a family history of CVD and preexisting CVD as modifiers of the stress responsiveness of plasma ET‐1, as reviewed by Yammine et al 8. Thus, an increase in plasma ET‐1 in response to stress is a physiological response that may be further amplified in the setting of vascular disease.…”

Section: Perspectivesmentioning

confidence: 99%

“…Prior studies have identified endothelin-1 (ET-1) as a psychosocial stress-responsive factor that may represent a mechanistic mediator of the connection between stress and CVD. 8 ET-1 is a nanomolar potent peptide produced by diverse cell types throughout the body that functions in autocrine and paracrine signaling. 9,10 Multiple studies have demonstrated an increase in plasma ET-1 levels in response to laboratory-induced acute psychosocial stress in healthy, at risk, and diseased human subjects.…”

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confidence: 99%

Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium‐Derived Endothelin‐1

Fox

Becker

Loria

et al. 2018

JAHA

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BackgroundAcute psychosocial stress provokes increases in circulating endothelin‐1 (ET‐1) levels in humans and animal models. However, key questions about the physiological function and cellular source of stress‐induced ET‐1 remain unanswered. We hypothesized that endothelium‐derived ET‐1 contributes to the acute pressor response to stress via activation of the endothelin A receptor.Methods and ResultsAdult male vascular endothelium‐specific ET‐1 knockout mice and control mice that were homozygous for the floxed allele were exposed to acute psychosocial stress in the form of cage switch stress (CSS), with blood pressure measured by telemetry. An acute pressor response was elicited by CSS in both genotypes; however, this response was significantly blunted in vascular endothelium‐specific ET‐1 knockout mice compared with control mice that were homozygous for the floxed allele. In mice pretreated for 3 days with the endothelin A antagonist, ABT‐627, or the dual endothelin A/B receptor antagonist, A‐182086, the pressor response to CSS was similar between genotypes. CSS significantly increased plasma ET‐1 levels in control mice that were homozygous for the floxed allele. CSS failed to elicit an increase in plasma ET‐1 in vascular endothelium‐specific ET‐1 knockout mice. Telemetry frequency domain analyses suggested similar autonomic responses to stress between genotypes, and isolated resistance arteries demonstrated similar sensitivity to α1‐adrenergic receptor‐mediated vasoconstriction.ConclusionsThese findings specify that acute stress‐induced activation of endothelium‐derived ET‐1 and subsequent endothelin A receptor activation is a novel mediator of the blood pressure response to acute psychosocial stress.

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Endothelin-1 and Psychosocial Risk Factors for Cardiovascular Disease

Cited by 19 publications

References 44 publications

The Predictive Value of Depressive Symptoms for All-Cause Mortality

The Predictive Value of Depressive Symptoms for All-Cause Mortality

Severe depressive symptoms are associated with elevated endothelin-1 in younger patients with acute coronary syndrome

Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium‐Derived Endothelin‐1

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