Increases in renal segmental artery vascular resistance acutely provoked by soft drink consumption are likely caused by high fructose corn syrup

Abstract

Regular excessive sugar‐sweetened soft drink consumption is associated with a higher risk of chronic kidney disease. Despite this association, relatively little is known about the acute physiological effects of soft drink consumption. High fructose corn syrup (HFCS) sweetened soft drinks elicit greater increases in blood pressure compared to soft drinks sweetened with sucrose. We have identified that, compared to drinking water, consuming a HFCS sweetened soft drink increases vascular resistance in the segmental arteries in the kidneys. It is unknown if this observation is unique to the HFCS in the soft drink or whether other beverage characteristics contributed to this response.PurposeTest the hypothesis that consuming a HFCS sweetened soft drink increases renal segmental artery vascular resistance compared to sucrose and artificially sweetened soft drinks, and water.MethodsTwelve healthy adults (24 ± 4 y, 2 females) participated in a randomized, double‐blind, quasi‐taste matched, crossover study. In four experimental trials, subjects drank 500 mL of a commercially available HFCS sweetened soft drink (HFCS, Mountain Dew®, osmolality: 846± 2 mOsm/kg), sucrose sweetened soft drink (SUCROSE, Mountain Dew Throwback®, osmolality: 730 ± 2 mOsm/kg), artificially sweetened soft drink (DIET, Diet Mountain Dew®, osmolality: 59 ± 2 mOsm/kg) and water (WATER, osmolality: 0 mOsm/kg) within a 5 min period. All soft drinks had a caffeine content of 77 mg. Data were collected following 20 min supine rest and 30 min post‐drinking. Blood pressure was measured in duplicate (sphygmomanometry). Renal and segmental artery blood velocities (BV) were obtained via Doppler ultrasound. Plasma osmolality was measured in venous blood samples. Vascular resistance (VR) in the renal and segmental arteries was calculated as mean arterial pressure (MAP) divided by BV. Data are presented as mean ± SD.ResultsThere were no differences between trials in MAP (P=0.90), renal artery BV (P=0.93) or VR (P=0.95), or segmental artery BV (P=0.32) or VR (P=0.28) pre‐drinking. Plasma osmolality increased post‐drinking of HFCS (by 2 ± 2 mOsm/kg, P=0.04) and SUCROSE (by 2 ± 2 mOsm/kg, P=0.04) but did not change with DIET (P=0.44) or WATER (P=0.98). MAP increased post‐drinking of SUCROSE (by 4 ± 4 mmHg, P=0.01) and DIET (by 4 ± 3 mmHg, P<0.01) but not with HFSC (P=0.17) or WATER (P>0.99). Renal artery BV increased post‐drinking of SUCROSE (by 2.6 ± 3.7 cm/s, P=0.04) but did not change with HFCS (P=0.43), DIET (P=0.99) or WATER (P=0.22). Renal artery VR did not change post‐drinking of HFCS (P=0.28), SUCROSE (P=0.31), DIET (P=0.77) or WATER (P=0.27). Drinking HFCS reduced segmental artery BV (by 1.6 ± 2.3 cm/s, P=0.01) but did not change with SUCROSE (P>0.99), DIET (P=0.99) or WATER (P=0.95). Segmental artery VR increased post‐drinking of HFCS (by 0.34 ± 0.55 mmHg/cm/s, P=0.02) but did not change with SUCROSE (P=0.96), DIET (P=0.67) or WATER (P=0.72).ConclusionAcute increases in renal segmental artery vascular resistance following soft drink consumption were likely caused by HFCS in these drinks, and not beverage osmolality or caffeine content.