Hypertension caused by high sugar intake is dose- and NO-dependent and inversely linked to GFR

This study tested the hypothesis that high sugar intake has a dose-dependent hypertensiveeffect that is exacerbated by blockade of NO synthesis. Six groups of rats were instrumentedwith chronic artery and vein catheters. Half the groups had chronic iv. L-NAME (L) infusion andhalf had vehicle infusion. All groups were fed a low-sucrose (LG) chow. On day G1, one vehicleand one L group were started on 66% high sucrose chow (HG), one of each group was startedon 66% sucrose chow plus iv. glucose infusion (VHG,~82% of calories from sugar), and theremaining 2 groups remained on the LG diet. Baseline MAP (24 hrs/day) in the 3 vehicle groupsaveraged 90±1, 86±1, and 92±1 mmHg in LG, HG, and VHG groups, respectively, and HG didnot increase MAP, just as we and others have shown with 66% fructose intake when MAP ismeasured 24 hrs/day. MAP also did not change in LG control rats, but VHG increased MAP~10 mmHg, also consistent with our previous reports. In the L-NAME groups, baseline MAPaveraged 115±1, 112±1, and 118±1 mmHg in the LG, HG, and VHG groups, respectively. The40 mmHg increase in MAP in the L+VHG rats is consistent with our previous report, but thekey test was the response in the HG rats: MAP increased by 22±6 mmHg in L+HG, comparedwith 2±1 mmHg in the HG rats, and no difference in blood glucose between groups; MAPincreased by 12±3 mmHg in the L+LG control rats. GFR averaged approximately 2.6, 2.5, and2.5 ml/min during week 2 in the LG, HG, and VHG vehicle rats, but was 2.3, 1.9, and 1.5 inthe L-NAME counterparts. These data show that 24 hr/day MAP is increased by high sugarintake in rats if NO synthesis is blocked chronically, and suggest that NO protects againsthypertension by preventing renal vasoconstriction