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Asia Pac J Clin Nutr. 2005;14(4):325-39.

Effect of palm oil on blood pressure, endothelial function and oxidative stress.

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Department of Pharmacology/Toxicology Morehouse School of Medicine, 720 Westview Drive, SW, Atlanta, Georgia 30310, USA.


The pathogenesis of hypertension has been associated with endothelial dysfunction and oxidative stress. We have previously shown that palm oil (PO), with an unsaturated-to-saturated fatty acid ratio close to one and rich in antioxidants vitamins, reduces oxidative stress-induced hypertension in normal rats. Here, we investigated the cardiovascular effects of natural vitamin-rich PO using the Dahl Salt-sensitive hypertension model. Male rats were fed either a high salt (8%NaCl, HS) or low salt (0.3% NaCl, LS) diet with or without PO (Carotino, 5 g/kg daily) for four weeks. Mean arterial pressure (MAP), heart rate, blood flow and vascular resistance, vascular reactivity in vitro as well as remodelling of second-order mesenteric arteries were measured. Plasma levels of nitric oxide (NO), prostacyclin, thromboxane A(2) (TXA(2)) and isoprostane (ISO), were determined by enzyme immunoassay. Plasma, heart and kidney GSH and GSSG levels were analyzed by HPLC and aortic superoxide ((.)O(2)-) production by fluorescence spectrometry. High salt induced an elevation in MAP that was associated with decreased NO, prostacyclin and GSH: GSSG ratio. Plasma ISO and TXA(2), aortic and renal vascular resistance as well as aortic (.)O(2)- were increased. Palm oil reduced MAP, plasma TXA(2) and vascular resistance of the renal and aortic arteries, and increased the GSH: GSSG ratio and NO in the LS group. The HS-induced elevation in ISO and (.)O(2)- production and the reductions in kidney GSH: GSSG ratio, were attenuated by PO. The effect of PO was also associated with a reduced vessel wall-thickness: lumen diameter ratio and a greater relaxant effect of mesenteric arteries to acetylcholine, in the LS group. The mortality associated with HS was reduced by PO. Thus, palm oil attenuates the progression of salt-induced hypertension and mortality, via mechanisms involving modulation of endothelial function and reduction in oxidative stress.

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