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Arterial endothelial function is impaired in treated depression.

ABSTRACT: OBJECTIVES:To determine whether patients with treated depression but no other risk factors for coronary heart disease (CHD) have abnormal arterial endothelial function, an abnormality that is common to other acquired risk factors for CHD. DESIGN:Case-control study. SETTING:Secondary care departments of cardiology and psychiatry in a single centre and the surrounding community. PARTICIPANTS:Patients with treated depression and matched healthy controls, aged 18-55 years, without conventional acquired risk factors for CHD. These were recruited from local community mental health clinics, general practices, and patient support groups, and through posters placed in public areas of the hospital. Patients had major depression as defined in the American Psychiatric Association's Diagnostic and statistical manual of mental disorders, fourth edition. Fifteen patients and 12 controls were recruited, and 12 patients and 10 controls completed the study. OUTCOMES:Brachial artery flow mediated dilatation and baroreflex sensitivity. RESULTS:Arterial endothelial function measured by flow mediated dilatation was impaired in depression (mean (SEM) -0.7% (1.7%)) compared with controls (5.7% (0.9%), p = 0.005 by non-paired t test). Baroreflex sensitivity did not differ significantly between the groups. CONCLUSION:Arterial endothelial function is impaired in treated depression. This abnormality may contribute to the increased risk of CHD seen in depression.

SUBMITTER: Broadley AJ

PROVIDER: S-EPMC1767404 | biostudies-literature | 2002 Nov

REPOSITORIES: biostudies-literature

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Arterial endothelial function is impaired in treated depression.

Broadley A J M AJ Korszun A A Jones C J H CJ Frenneaux M P MP

Heart (British Cardiac Society) 20021101 5

<h4>Objectives</h4>To determine whether patients with treated depression but no other risk factors for coronary heart disease (CHD) have abnormal arterial endothelial function, an abnormality that is common to other acquired risk factors for CHD.<h4>Design</h4>Case-control study.<h4>Setting</h4>Secondary care departments of cardiology and psychiatry in a single centre and the surrounding community.<h4>Participants</h4>Patients with treated depression and matched healthy controls, aged 18-55 year ...[more]

PMID: 12381649

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Project description:We aimed to characterize circulating microparticles in association with arterial stiffness, inflammation and endothelial dysfunction in aldosterone-salt-induced hypertension in rats and to investigate the preventive effects of red wine polyphenols. Uninephrectomized male Sprague-Dawley rats were treated with aldosterone-salt (1 µg.h(-1)), with or without administration of either red wine polyphenols, Provinols™ (20 mg.kg(-1).day(-1)), or spironolactone (30 mg.kg(-1).day(-1)) for 4 weeks. Microparticles, arterial stiffness, nitric oxide (NO) spin trapping, and mesenteric arterial function were measured. Aldosterone-salt rats showed increased microparticle levels, including those originating from platelets, endothelium and erythrocytes. Hypertension resulted in enhanced aortic stiffness accompanied by increased circulating and aortic NO levels and an upregulation of aortic inducible NO-synthase, NFκB, superoxide anions and nitrotyrosine. Flow-induced dilatation was reduced in mesenteric arteries. These effects were prevented by spironolactone. Provinols™ did not reduce arterial stiffness or systolic hypertension but had effects similar to those of spironolactone on endothelial function assessed by flow-mediated vasodilatation, microparticle generation, aortic NO levels and oxidative stress and apoptosis in the vessel wall. Neither the contractile response nor endothelium-dependent relaxation in mesenteric arteries differed between groups. The in vivo effects of Provinols™ were not mediated by mineralocorticoid receptors or changes in shear stress. In conclusion, vascular remodelling and endothelial dysfunction in aldosterone-salt-mediated hypertension are associated with increased circulating microparticles. Polyphenols prevent the enhanced release of microparticles, macrovascular inflammation and oxidative stress, and microvascular endothelial dysfunction independently of blood pressure, shear stress and mineralocorticoid receptor activation in a model of hyperaldosteronism.

Dataset Information

Arterial endothelial function is impaired in treated depression.

Publications

Arterial endothelial function is impaired in treated depression.

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