Coconut oil has been used as a source of fatty acids since ancient times. However, its major chemical components are saturated fatty acids and these are now considered to be a health hazard, especially to the cardiovascular system. In this study we aimed to test for any harmful effects of feeding virgin coconut oil on the cardiovascular system of middle-aged rats. Tests included (1) blood sugar and lipid profiles, (2) basal blood pressure and heart rate, and (3) isolated blood vessel functions. The saturated fatty acid composition (%) of the virgin coconut oil (VCO, Thai pure coconut Co., Thailand) was: C8, 4.7; C10, 6.2; C12 (lauric acid), 51.9; C14, 18.2; C16, 6.9 and C18, 1.9. Middle-aged male rats (14-15 months old) were gavaged with 1 or 3 ml VCO /kg or distilled water (control), once a day for 6 weeks. Basal blood pressure and heart rate were measured from anesthetized rats (sodium pentobarbital, 60 mg/kg, i.p) via the right common carotid artery. Blood sugar and lipids profile were measured by enzymatic methods. The thoracic aorta was isolated from rats decapitated with a guillotine, then placed in oxygenated Krebs Heinseleit solution at 37oC (PSU-Ethic No.10/54) before performing a cumulative concentration response (C-R) curve to phenylephrine (Phe), acetylcholine (ACh) and glyceryl trinitrate (GTN). Data are expressed as a mean ± S.E.M. (6 rats/group/each experiment). Using the Student’s paired t-test, a p ≤ 0.05 between test and control was considered to be statistically significant. After 6 weeks of treatment with 1 or 3 ml of VCO/kg, there were no changes in serum glucose and lipid profiles, mean arterial blood pressure and heart rate when compared to the control group. There were no significant changes in vascular responses to Phe, ACh and GTN for the dosage of 1 ml/kg VCO. At a dosage of VCO of 3 ml/kg, the maximal contractile responses of the endothelium-intact thoracic aortic ring, with or without N-nitro-L-arginine (LNA, 300 µM)), a nitric oxide synthase inhibitor, to Phe was significantly lower than the one obtained from the control group. Also the vasodilatory response to ACh by the endothelium-intact aortic ring preconstricted with Phe (3 µM) was significantly higher than the control group. This effect disappeared when the blood vessels had been incubated with LNA or tetraethylammonium (1 mM) but not by glybenclamide (10 µM). The vasodilatation to GTN was not different from the control for the endothelium-intact thoracic aortic ring treated with LNA. These results indicate that consumption of the virgin coconut oil of 1-3 ml/kg/day had some beneficial effects on the cardiovascular system of the middle-aged male rats by increasing the release of nitric oxide from the vascular endothelium and opening of the Kca channels to cause a higher vasodilatation to ACh and to oppose the vasoconstriction produced Phe.