Over the last half century fructose has become an important component of the human diet in the industrialized countries, mainly in the form of added sugars which are added to food during its manufacture and processing. Recently it was shown that high fructose intake might evoke some cardiometabolic aberrations in predisposed individuals. In this study we assessed the effects of fructose administration to rat strains with different levels of cardiovascular impairment. High doses of fructose (as 10% solution replacing drinking water) were administered for eight weeks to 12-week-old male rats that include normotensive Wistar rats, Wistar rats receiving 40 mg/kg/day of N^G-nitro-L-arginine methyl ester to evoke nitric oxide (NO) deficiency, and spontaneously hypertensive rats (SHR). We found that fructose administration induced an increase in plasma glucose and triglycerides, elevation of blood pressure, and impairment of arterial endothelium-dependent relaxation in normotensive Wistar rats and in SHR but not in hypertensive NO-deficient rats, when compared to their respective control (non-fructose drinking) groups. Treatment with fructose led to the reduction of arterial contractile force in response to noradrenergic stimulation in SHR and in hypertensive NO-deficient rats but not in normotensive Wistar rats. Our results show that fructose consumed in excess evokes some features of metabolic syndrome in normotensive rats and SHR at similar degrees and that deficiency of NO in rats prevents the development of most of the abnormalities induced by fructose administration.