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

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

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Prüfsumme: MD5:7c4a1583c63a8a158b72f88ef75c9661

WIRTZ, Petra H., Ulrike EHLERT, Carmen BÄRTSCHI, Laura S. REDWINE, Roland VON KÄNEL, 2009. Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response. In: Metabolism. 58(1), pp. 30-37. ISSN 0026-0495. eISSN 1532-8600

@article{Wirtz2009Chang-30681, title={Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response}, year={2009}, doi={10.1016/j.metabol.2008.08.003}, number={1}, volume={58}, issn={0026-0495}, journal={Metabolism}, pages={30--37}, author={Wirtz, Petra H. and Ehlert, Ulrike and Bärtschi, Carmen and Redwine, Laura S. and von Känel, Roland} }

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. eng Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response 2009 Bärtschi, Carmen von Känel, Roland 2015-04-08T08:15:07Z Redwine, Laura S. von Känel, Roland Wirtz, Petra H. Ehlert, Ulrike 2015-04-08T08:15:07Z Redwine, Laura S. Bärtschi, Carmen Wirtz, Petra H. Ehlert, Ulrike

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