Longchain n−3 polyunsaturated fatty acids and blood vessel function

Abstract

The cardiovascular health benefits of longchain n-3 polyunsaturated fatty acids (PUFAs) have been reported to exert at several different cellular control mechanisms. These include, effects on lipoprotein metabolism, haemostatic function, platelet/vessel wall interactions, anti-arrhythmic actions and also inhibition of proliferation of smooth muscle cells and therefore growth of the atherosclerotic plaque. Fish oil feeding has also been found to result in moderate reductions in blood pressure and to modify vascular neuroeffector mechanisms. The majority of such cardiovascular benefits of n-3 PUFAs are likely to be mediated in the vascular wall and at the vascular endothelium level, since this monolayer of cells plays a central role in the regulation and maintenance of cardiovascular homeostasis and function. While these processes include endothelium-derived vasorelaxant and vasoconstrictor compounds, the vascular endothelium also plays host to many receptors, binding proteins, transporters and signalling mechanisms. Accordingly, endothelial dysfunction, which underlies many cardiovascular disease conditions, can trigger acute vascular events including vasospasm, thrombosis or restenosis leading to ischaemia. The longchain n-3 PUFAs have been reported to possess several properties that may positively influence vascular function. These include favourable mediator profiles (nitric oxide, eicosanoids) that influence vascular reactivity, change in vascular tone via actions on selective ion channels, and maintenance of vascular integrity. In addition to direct effects on contractility, n-3 PUFAs may affect vascular function, and the process of atherogenesis, via inhibition of vascular smooth muscle cell proliferation at the gene expression level, and by modifying expression of inflammatory cytokinesis and adhesion molecules. Collectively, these properties are consistent with pleiotropic actions of longchain n-3 PUFAs, and may explain the beneficial cardiovascular protection of this family of fatty acids that have been clearly evident through epidemiological data as well from more recent large-scale clinical trials.

Kinetics of chronic inflammation in Nile tilapia fed n‑3 and n‑6 essential fatty acids

“…The increased Langhans giant cell formation on the sixth and eighth days of inflammation observed in Nile tilapia supplemented with 100% linseed shows the participation of n-3 fatty acids in the physiopathology of these processes, increasing the macrophage activity. Additionally, fatty acids that modulate immune responses and eicosanoids produced from arachidonic acid (20:4n-6) are recognized as inflammatory agents (Abeywardena & Head, 2001;Ganga et al, 2005;Calder, 2006).…”

Dietary intake of n-3, n-6 fatty acids and fish: Relationship with hostility in young adults—the CARDIA study

“…There are several potential mechanisms for this protection including antithrombotic (Kristensen et al, 1989;Prisco et al, 1995) and anti-arrhythmic effects (Marchioli et al, 2002), decreased heart rate variability (Christensen et al, 1997) and resting blood pressure (Knapp, 1989), decreased serum LDL cholesterol and triglyceride concentrations (Agren et al, 1996) and increased insulin sensitivity (Torjesen et al, 1997;Mori et al, 1999). Other plausible but less-explored mechanisms by which dietary fish or n-3 polyunsaturated fatty acids may be beneficial for cardiovascular health are favorable effects on endothelial function (Abeywardena & Head, 2001), anti-inflammatory effects (Madsen et al, 2001) as well as neuroendocrine influences including modulation of the hypothalamic-pituitary-adrenocortical axis activity (Wang et al, 1999).…”

Polyunsaturated fatty acid intake and blood pressure in adolescents

“…4 We observed small correlations between PUFA intake and RBC fatty acids, and it is likely that the lipid composition of cell membranes is one aspect contributing to BP. 28 Other ways that PUFAs are likely to affect BP include alteration of eicosanoid synthesis, endothelial function, vascular reactivity and nitric oxide production. 28 In addition, different classes of PUFAs may exert more specific effects on BP through varying mechanisms.…”

“…28 Other ways that PUFAs are likely to affect BP include alteration of eicosanoid synthesis, endothelial function, vascular reactivity and nitric oxide production. 28 In addition, different classes of PUFAs may exert more specific effects on BP through varying mechanisms. 5 Although both EPA and DHA showed independent inverse associations with measures of BP, we observed slightly stronger relationships with EPA than DHA in boys.…”