Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

Wirtz, Petra H.; Ehlert, Ulrike; Bärtschi, Carmen; Redwine, Laura S; von Känel, Roland (2009). Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response. Metabolism, 58(1), pp. 30-7. Orlando, Fla.: Elsevier 10.1016/j.metabol.2008.08.003

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Hypertension is a known risk factor for cardiovascular disease. Hypertensive individuals show exaggerated norepinephrine (NE) reactivity to stress. Norepinephrine is a known lipolytic factor. It is unclear if, in hypertensive individuals, stress-induced increases in NE are linked with the elevations in stress-induced circulating lipid levels. Such a mechanism could have implications for atherosclerotic plaque formation. In a cross-sectional, quasi-experimentally controlled study, 22 hypertensive and 23 normotensive men (mean +/- SEM, 45 +/- 3 years) underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma NE and the plasma lipid profile (total cholesterol [TC], low-density-lipoprotein cholesterol [LDL-C], high-density-lipoprotein cholesterol, and triglycerides) immediately before and after stress and at 20 and 60 minutes of recovery. All lipid levels were corrected for stress hemoconcentration. Compared with normotensives, hypertensives had greater TC (P = .030) and LDL-C (P = .037) stress responses. Independent of each other, mean arterial pressure (MAP) upon screening and immediate increase in NE predicted immediate stress change in TC (MAP: beta = .41, P = .003; NE: beta = .35, P = .010) and LDL-C (MAP: beta = .32, P = .024; NE: beta = .38, P = .008). Mean arterial pressure alone predicted triglycerides stress change (beta = .32, P = .043) independent of NE stress change, age, and BMI. The MAP-by-NE interaction independently predicted immediate stress change of high-density-lipoprotein cholesterol (beta = -.58, P < .001) and of LDL-C (beta = -.25, P < .08). We conclude that MAP and NE stress reactivity may elicit proatherogenic changes of plasma lipids in response to acute psychosocial stress, providing one mechanism by which stress might increase cardiovascular risk in hypertension.

Item Type:

Journal Article (Original Article)

Division/Institute:

07 Faculty of Human Sciences > Institute of Psychology > Clinical Psychology and Psychotherapy
04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurology > Centre of Competence for Psychosomatic Medicine

UniBE Contributor:

Wirtz, Petra Hedwig and von Känel, Roland

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0026-0495

Publisher:

Elsevier

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 15:15

Last Modified:

21 Sep 2017 17:15

Publisher DOI:

10.1016/j.metabol.2008.08.003

PubMed ID:

19059528

Web of Science ID:

000261975200005

URI:

https://boris.unibe.ch/id/eprint/33436 (FactScience: 198977)

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