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Kidney Week

Abstract: TH-PO507

Sodium Thiosulfate Improves Renal Function and Oxygenation in L-NNA Induced Hypertensive Rats

Session Information

  • CKD: Mechanisms - I
    November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms


  • Nguyen, Isabel T.N., University Medical Center Utrecht, Utrecht, Netherlands
  • Klooster, Astrid, Pathologie Friesland, Leeuwarden, Netherlands
  • Feelisch, Martin, University of Southampton, Southampton, United Kingdom
  • Verhaar, Marianne C., University Medical Center Utrecht, Utrecht, Netherlands
  • Van goor, Harry, UMCG, Groningen, Netherlands
  • Joles, Jaap A., University Medical Center Utrecht, Utrecht, Netherlands

Sodium thiosulfate (STS, Na2S2O3), a H2S donor, a vasodilator and anti-oxidant, is an attractive agent for alleviating the damaging effects of hypertension. In experimental setting, nitric oxide synthase (NOS) inhibition by L-NNA induces hypertension, renal dysfunction and damage. We hypothesized that 1) STS attenuates renal injury and improves renal function, hemodynamics and oxygen efficiency in hypertensive renal disease and that 2) STS on top of RAS inhibition will further improve aforementioned variables in comparison to RAS inhibition alone.


NOS was inhibited in male Sprague Dawley rats by administering L-NNA (40 mg/kg/day) in the food for 3 weeks. After one week of NOS inhibition, rats were split in 2 groups for the remaining 2 weeks, 1) L-NNA only and 2) L-NNA with STS (2 g/kg/day) in the drinking water. In a parallel study, rats were divided in 2 groups, 1) L-NNA with lisinopril (1mg/kg/day) mixed in the food and 2) L-NNA with both lisinopril and STS. After weekly systolic blood pressure measurements and 24h urine collection, hemodynamics and sodium reabsorption efficiency (TNa/QO2, sodium reabsorbed per oxygen consumed) were assessed under isoflurane and kidneys were collected for glomerulosclerosis and mesangial matrix expansion scores.


STS increased 24h excretions of sodium 3.5-fold and sulphate 30-fold, alleviated hypertension (165±5 vs. 228±5 mmHg, P<0.001), reduced plasma urea (11±1 vs. 21±4 mmol/L, P<0.05) and improved terminal GFR (503±25 vs. 260±45 μl/min/100 g BW, P<0.01), effective renal plasma flow (919±64 vs. 532±97 μl/min/100 g BW, P<0.01) and TNa/QO2 (14.3±1.1 vs. 8.6±1.4 μmol/μmol, P<0.01). Combining STS with lisinopril further reduced renal vascular resistance (43±4 vs. 63±7 mmHg/ml/min/100 g BW, P<0.05) vs. L-NNA+lisinopril. Additionally, glomerulosclerosis was completely prevented (P<0.001) and mesangial matrix expansion (P<0.01) was markedly reduced in L-NNA+lisinopril+STS vs. L-NNA+lisinopril.


Our results suggest that supplementing H2S has therapeutic potential in hypertensive renal disease and might be of additive value in already existing antihypertensive regimens despite the increase in sodium load.


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