We first tested the hypothesis that consuming a high-fructose corn syrup (HFCS)-sweetened soft drink augments kidney vasoconstriction to sympathetic stimulation compared with water ( study 1). In a second study, we examined the mechanisms underlying these observations ( study 2). In study 1, 13 healthy adults completed a cold pressor test, a sympathoexcitatory maneuver, before (preconsumption) and 30 min after drinking 500 mL of decarbonated HFCS-sweetened soft drink or water (postconsumption). In study 2, venous blood samples were obtained in 12 healthy adults before and 30 min after consumption of 500 mL water or soft drinks matched for caffeine content and taste, which were either artificially sweetened (Diet trial), sucrose-sweetened (Sucrose trial), or sweetened with HFCS (HFCS trial). In both study 1 and study 2, vascular resistance was calculated as mean arterial pressure divided by blood velocity, which was measured via Doppler ultrasound in renal and segmental arteries. In study 1, HFCS consumption increased vascular resistance in the segmental artery at rest (by 0.5 ± 0.6 mmHg·cm−1·s−1, P = 0.01) and during the cold pressor test (average change: 0.5 ± 1.0 mmHg·cm−1·s−1, main effect: P = 0.05). In study 2, segmental artery vascular resistance increased in the HFCS trial (by 0.8 ± 0.7 mmHg·cm−1·s−1, P = 0.02) but not in the other trials. Increases in serum uric acid were greater in the HFCS trial (0.3 ± 0.4 mg/dL, P ≤ 0.04) compared with the Water and Diet trials, and serum copeptin increased in the HFCS trial (by 0.8 ± 1.0 pmol/L, P = 0.06). These findings indicate that HFCS acutely increases vascular resistance in the kidneys, independent of caffeine content and beverage osmolality, which likely occurs via simultaneous elevations in circulating uric acid and vasopressin.

BackgroundIncreases in dietary fructose are associated with a greater risk of renal disease. Fructose consumption promotes the release of vasopressin, stimulates uric acid production, and elevates blood pressure. Consumption of a high‐fructose, caffeinated soft drink acutely reduces kidney function during exercise in the heat. These reductions were likely caused by elevations in circulating vasopressin and uric acid, which have vasoconstrictor actions in the kidneys. Thus, it is possible that soft drink‐mediated reductions in renal blood flow contributed to the reduced kidney function. However, the effect of soft drink consumption on the renal vasoconstrictor response is unknown.PurposeThe cold pressor test (CPT) is a sympathetic stimulus that can be used to examine renal vasoconstrictor responsiveness. This study tested the hypothesis that soft drink consumption exacerbates the increase in renal vascular resistance (RVR) to the CPT.MethodsEleven euhydrated healthy adults (22 ± 2 y, 3 F) completed a CPT by immersing their right hand in an agitated ice slurry mixture for 2 min, 1 h after drinking 250 mL of tap water (Water) and again 30 min following consumption of 500 mL of decarbonated Mountain Dew® (Soft Drink). Heart rate (3 lead ECG), mean arterial pressure (MAP, finger photoplethysmography), and renal blood velocity (RBV, n=8) were measured at 1 min pre‐CPT, at 1 and 2 min into the CPT (CPT1 and CPT2), and 1 min post‐CPT. RBV was assessed in the same location of the same segmental artery during the same phase of the respiratory cycle via Doppler ultrasound (GE Vivid iQ). The coronal approach was utilized using a linear‐array transducer with a 2.5 MHz pulsed frequency while participants were in the left lateral recumbent position. All measurements were obtained by the same sonographer (intraoperator coefficient of variation: 3.8 ± 0.9%) with the focal zone set to the artery's depth, and the transducer held in the same location at an insonation angle <60°. RVR was calculated as MAP/RBV. RBV and RVR were averaged across three cardiac cycles.ResultsHeart rate was not different between Water (61 ± 10 bpm) and Soft Drink (65 ± 10 bpm) at pre‐CPT (P=0.14). Heart rate increased during the CPT (P=0.01), but there were no differences between Water and Soft Drink (P≥0.35). MAP was not different between Water (76 ± 10 mmHg) and Soft Drink (79 ± 13 mmHg) at pre‐CPT (P=0.62). MAP increased with the CPT (P<0.01), and was higher in Soft Drink at CPT1 (104 ± 13 vs. 98 ± 12 mmHg, P=0.04) and post‐CPT (90 ± 13 vs. 80 ± 12 mmHg, P<0.01), with no differences between Water (106 ± 13 mmHg) and Soft Drink (106 ± 11 mmHg) at CPT2 (P=0.99). RBV was lower in Soft Drink throughout (20.8 ± 1.2 vs. 18.3 ± 0.4 cm/s, main effect: P<0.01), and did not change during the CPT in Water or Soft Drink (P=0.64). RVR was elevated at pre‐CPT in Soft Drink (4.5 ± 1.3 vs. 3.9 ± 1.0 mmHg/cm/s, P=0.05). RVR increased during the CPT in Water and Soft Drink (P<0.01), and was higher in Soft Drink at CPT1 (6.1 ± 1.3 vs. 5.0 ± 1.3 mmHg, P<0.01) and at post‐CPT (5.3 ± 1.5 vs. 3.8 ± 1.3 mmHg, P<0.01), with no differences between Water (5.5 ± 1.6 mmHg) and Soft Drink (6.0 ± 1.6 mmHg) at CPT2 (P=0.13).ConclusionSoft drink consumption augments the renal vasoconstrictor response to a sympathetic stimulus.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.