Fructose feeding in rats is not associated with sodium retention

Chronic fructose treatment in rats repeatedly has been shown to elevate blood pressure associated with insulin resistance and hyperinsulinemia. Activation of the sympathetic nervous system and the renin-angiotensin system, vascular hypertrophy, and sodium retention by the kidney tubules have been proposed to be some of the mechanisms by which insulin elevates blood pressure. The precise mechanism by which hypertension develops in fructose-fed rats is still not known. The purpose of the current study was twofold. The first objective was to assess the effect of a fructose-enriched diet on urinary sodium excretion. The second objective was to investigate any changes in plasma volume and extracellular volume in fructose-fed rats. In both experiments, male Sprague-Dawley rats were divided into equal groups. Rats in the control group were fed Purina Laboratory Chow, whereas those in the experimental group were fed a 60% fructose diet. There was a significant elevation in the blood pressure of fructose-fed rats at the end of the second week of treatment, and it remained elevated for the remainder of the dietary intervention. In the first experiment, there was no significant difference in sodium, potassium or urine excretion throughout the 6 weeks of dietary treatment. At the end of this study, the serum insulin levels of fructose-fed rats were significantly greater than the levels in the control group. In the second experiment, which was a 4-week study, there was no significant difference in hematocrit, plasma volume, or extracellular fluid volume between control and fructose-fed animals at 2 or 4 weeks of dietary treatment. The results of these two in vivo studies are the first to document that elevation of blood pressure in fructose-fed rats does not occur directly via sodium retention or an increase in fluid volume.