Objectives: 

Long-term excessive fructose intake induces the features of metabolic syndrome in animals as well as in humans. The goal of this study was to analyze the magnitude of cardiovascular impairment due to high-fructose feeding in two different rat strains, one of them with genetically-induced hypertension.

Materials: 

Experiments were performed on male twelve-week-old normotensive Wistar and spontaneously hypertensive rats (SHR) divided randomly into two groups: control group drinking just tap water, and a group given water containing 10 % fructose. Systolic blood pressure was measured by a tail-cuff method in conscious animals. In 20th week of age, all rats were sacrificed and plasma concentrations of triglycerides, total cholesterol and glucose were measured. Rings of isolated thoracic aorta and mesenteric artery were suspended in organ baths containing modified Krebs solution and connected to a force-displacement transducer for the recording of isometric tension. Neurogenic contractions were elicited by electrical stimulation of perivascular adrenergic nerves.

Results: 

Fructose feeding induced weight gain and elevation of blood pressure in SHR, but not in normotensive Wistar rats. In both rat strains, this treatment resulted in increase of relative liver weight and plasma triglycerides. Endothelium-dependent relaxations to acetylcholine and contractions to noradrenaline were diminished in aortic rings from fructose-fed SHR, but not in that from Wistar rats. Moreover, in SHR high fructose intake blunted sensitivity to noradrenaline in the aorta and supressed neurogenic responses in the mesenteric artery elicited by stimulation of perivascular adrenergic nerves.

Conclusions: 

These results showed that the metabolic changes induced by high-fructose feeding had no impact on cardiovascular function in normotensive Wistar rats. In contrast, fructose administration to SHR led to further blood pressure increase and impairment of vascular function.

Supported by grant VEGA No. 2/0188/12.