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Proximal tubule fructose metabolism is key to fructose-induced hypertension, but the roles of sex and stress are unclear. We hypothesized that females are resistant to the salt-sensitive hypertension caused by low amounts of dietary fructose compared to males and that the magnitude of the increase in blood pressure (BP) depends, in part, on amplification of the stress response of renal sympathetic nerves. We measured systolic BP (SBP) in rats fed high salt with either no sugar (HS), 20% glucose (GHS) or 20% fructose (FHS) in the drinking water for 7-8 days. FHS increased SBP (p<0.03 vs basal) but neither GHS nor high salt alone raised SBP. FHS increased SBP significantly and similarly in both (male: Δ25±8 mm Hg; female: Δ19±2 mm Hg). FHS increased SBP by 24±5 mm Hg but only by 8±2 mm Hg when measured by plethysmography and telemetry, respectively (p<0.004). When SBP was measured by telemetry under low stress, FHS increased SBP by 8±1 mm Hg; on the contrary, when measured by telemetry under moderate stress conditions (simulating stress of plethysmography), FHS increased SBP by 15±3 mm Hg, a significantly greater increase (p<0.008). Norepinephrine excretion in rats subjected to moderate stress was 63±17 nmole/Kg/day for animals fed FHS but only 19±40 nmole/Kg/day for controls fed HS (p<0.02). We conclude that fructose-induced salt-sensitive hypertension is similar in males and females unlike other forms of hypertension, and the increase in blood pressure depends in part on an augmented response of the sympathetic nervous system to stress.
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