1988
DOI: 10.1016/0026-0495(88)90145-x
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Effects of catecholamines on serum lipoproteins of normally fed and cholesterol-fed rabbits

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Cited by 22 publications
(9 citation statements)
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“…Consistent with the results of the present study, the relative contributions of the two opposing pathways are therefore determined by levels of p-NE. Furthermore, the finding of p-NE being associated with p-lipids (cholesterol, LDL, HDL and triglycerides) is in line with results of previous studies on the role of catecholamines in the regulation of lipid metabolism (O'Donnell et al, 1988;Petrak et al, 2013). The observed direct relationship between p-NE, cholesterol, LDL and triglycerides as well as the inverse relationship between p-NE and HDL suggest that increased SNS activity may increase the risk of CVD (Mottillo et al, 2010).…”
Section: Discussionsupporting
confidence: 79%
“…Consistent with the results of the present study, the relative contributions of the two opposing pathways are therefore determined by levels of p-NE. Furthermore, the finding of p-NE being associated with p-lipids (cholesterol, LDL, HDL and triglycerides) is in line with results of previous studies on the role of catecholamines in the regulation of lipid metabolism (O'Donnell et al, 1988;Petrak et al, 2013). The observed direct relationship between p-NE, cholesterol, LDL and triglycerides as well as the inverse relationship between p-NE and HDL suggest that increased SNS activity may increase the risk of CVD (Mottillo et al, 2010).…”
Section: Discussionsupporting
confidence: 79%
“…Blood pressure reactivity was associated with atherosclerosis independently of standard risk factors. A number of possible mechanisms could underlie the association of blood pressure reactivity and carotid IMT thickening 11,25,26 and are derived from the known influences of mental stress and the consequent effect of exaggerated hemodynamic responses to these stressors: (1) hyperdynamic circulatory changes may be injurious to the endothelial lining of coronary vessels, 27 (2) sympatheticoadrenal activation may contribute to vasospasm, 28 (3) adrenomedullary and adrenocortical responses may contribute to lipid mobilization, platelet aggregation, or both, 29,30 and (4) mental stress may induce immunologic responses that may have an impact on coronary artery plaque development. 31 A diathesis-stress model 11,26 suggests that these processes may be the most potent among individuals who not only show exaggerated reactivity but also experience chronic exposure to stress.…”
Section: Discussionmentioning
confidence: 99%
“…For example, sympathetic arousal contributes to injury and dysfunction of the arterial endothelium, which may lead to formation of atherosclerotic plaques. 13,31 In addition, neuroendocrine correlates of sympathetic nervous system activation, including increases in norepinephrine, epinephrine, and cortisol, can promote lipid mobilization 32,33 and platelet activation, contributing to aggregation of platelets and formation of thrombi. 34 Both of these processes also may exacerbate vascular injury and atherosclerotic plaque formation and progression.…”
Section: Discussionmentioning
confidence: 99%