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Abstract: FR-PO403

Effects of Mild Hyperuricemia in the Progression of Salt-Sensitive Hypertension and Associated Kidney Damage

Session Information

  • Hypertension and CVD: Basic
    November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Hypertension and CVD

  • 1601 Hypertension and CVD: Basic


  • Dissanayake, Lashodya Vindana, University of South Florida, Tampa, Florida, United States
  • Zietara, Adrian P., University of South Florida, Tampa, Florida, United States
  • Levchenko, Vladislav, University of South Florida, Tampa, Florida, United States
  • Palygin, Oleg, Medical University of South Carolina, Charleston, South Carolina, United States
  • Staruschenko, Alexander, University of South Florida, Tampa, Florida, United States

Increased plasma uric acid (UA) (hyperuricemia (HrU)) causes damage via crystal deposition throughout the body in gout. HrU is also a potential causal factor in hypertension (HTN) & chronic kidney disease (CKD). Whether only HrU with crystals, but not asymptomatic HrU (HrU without crystal deposition), drives the progression of HTN & CKD is controversial. Additionally, dietary salt intake is involved in blood pressure & renal function control & may affect UA levels. The renin-angiotensin-aldosterone system (RAAS) activation may trigger HTN during HrU; however, lowering UA did not affect RAAS activity in some clinical studies.


To answer the question if asymptomatic HrU in the context of salt sensitivity (SS) is a friend or foe, we explored conditions of induced mild HrU & a high salt diet on the development of HTN using Dahl SS rats & administration of either oxonic acid, a uricase inhibitor that prevents the breakdown of UA further into more soluble allantoin &/or probenecid, an inhibitor of the UA transporter Urat1, preventing UA reuptake. 8-week-old male rats were implanted with telemeters to assess mean arterial pressure (MAP). After recovery, SS rats were switched to one of 4 diets: 1) 4% NaCl high salt (HS) diet (control, N=6); 2) HS + 2% oxonic acid (treatment 1, N=7); 3) HS + 750 mg/kg Probenecid (treatment 2, N=4); or 4) HS + 750 mg/kg Probenecid + 2 % oxonic acid (treatment 3, N=3) for 3 weeks.


At the endpoint, treatment group 1 had significantly higher plasma UA levels compared to the control group (2.17±0.34 vs. 0.63±0.07 mg/dl). This mild HrU was associated with attenuated progression of SS HTN while probenecid did not affect MAP & diminished the effect of oxonic acid (MAP for control & treatment 1-3 groups: 156±3, 138±3, 162±3, & 154±4 mmHg). Treatment group 1 also had a lower kidney weight/body weight ratio & lower protein cast accumulation, indicating lower kidney damage. Assessment of circulating RAAS hormones showed no treatment-specific changes.


These results indicate mild HrU in Dahl SS rats attenuates HTN & renal damage without affecting RAAS. Our data suggest that HrU is not inherently detrimental but beneficial to cardiovascular & kidney health under certain conditions.


  • Other NIH Support