SUMMARY To determine if hypertension could be produced in normal rats by feeding them a fructose-enriched diet, Sprague-Dawley rats were fed either normal chow or a diet containing 66% fructose as a percentage of total calories for approximately 2 weeks. At the end of this period systolic blood pressure had increased from 124 ± 2 to 145 ± 2 (SEM) mm Hg in the fructose-fed rats, whereas no change occurred in the control group. In addition, hyperinsulinemia and hypertriglyceridemia were associated with hypertension in fructose-fed rats. The addition of clonidine to the drinking water inhibited fructose-induced hypertension, but not the increase in plasma insulin or triglyceride concentration seen in fructose-fed rats. Thus, the metabolic changes associated with fructose-induced hypertension are unlikely to be secondary to an increase in sympathetic activity. Whether or not this is also true of the hypertension remains to be clarified. IT has been apparent for some time that increases in dietary carbohydrate intake can raise blood pressure in experimental animals. '• 2 In particular, the ability of sucrose feeding to accentuate the magnitude of the blood pressure elevation already present in spontaneously hypertensive rats has been documented. 3 " 3 Since sucrose feeding stimulates sympathetic nervous system activity, 6 it has been suggested that sucroseinduced increases in sympathetic activity may elevate blood pressure in susceptible animals.4 Indirect support for this hypothesis was provided by the observation that rats with sucrose-induced hypertension had faster heart rates and larger hypotensive responses to a-adrenergic blockade with phentolamine than did their normotensive controls.7 This point of view has recently received added support from the demonstration that hypertension produced by sucrose feeding is associated with evidence of increased catecholamine Received March 13, 1987; accepted June 21, 1987. secretion. 5 However, the physiological effects of sucrose are not limited to an increase in sympathetic activity, and rats fed a high sucrose diet also become insulin-resistant and hyperinsulinemic.8 ' 9 Since several recent observations have documented an association between hyperinsulinemia and hypertension in humans, 10 " 12 it seemed important to see if a similar phenomenon could be found in carbohydrate-induced hypertension in rats. Thus, the current study was initiated to address this issue, and we have taken a somewhat different approach than has been conventionally used in an effort to broaden the nature of inquiry. First, we used normal Sprague-Dawley rats, not animals with spontaneous hypertension, to see if high carbohydrate diets can induce hypertension in rats with no apparent genetic propensity to become hypertensive. Second, we used fructose, not sucrose, as the source of dietary carbohydrate. Fructose feeding can also cause insulin resistance and hyperinsulinemia in normal rats.'14 If fructose also produces hypertension, it would suggest that the insulin resistance and hyperinsu...

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