Longchain n-3 polyunsaturated fatty acids and blood vessel function.
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.
Abeywardena
M Y
MY
CSIRO Health Sciences and Nutrition, Kintore Avenue, P.O. Box 10041, BC, SA 5000, Adelaide, Australia. mahinda.abeywardena@hsn.csiro.au
Head
R J
RJ
D000889:Anti-Arrhythmia Agents; D001161:Arteriosclerosis / Q000188:drug therapy / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002455:Cell Division; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D016207:Cytokines / Q000378:metabolism; D015777:Eicosanoids / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism; D015525:Fatty Acids, Omega-3 / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D005343:Fibrinolytic Agents; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D007962:Leukocytes / Q000473:pathology; D009200:Myocardial Contraction / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects*
D000889:Anti-Arrhythmia Agents; D015815:Cell Adhesion Molecules; D016207:Cytokines; D015777:Eicosanoids; D015525:Fatty Acids, Omega-3; D005343:Fibrinolytic Agents; D007473:Ion Channels; D009569:Nitric Oxide; D011464:Epoprostenol