2. Academic Validation
  3. Sodium Thiosulfate Improves Hypertension in Rats with Adenine-Induced Chronic Kidney Disease

Sodium Thiosulfate Improves Hypertension in Rats with Adenine-Induced Chronic Kidney Disease

  • Antioxidants (Basel). 2022 Jan 11;11(1):147. doi: 10.3390/antiox11010147.
Chien-Ning Hsu 1 2,  Chih-Yao Hou 3,  Guo-Ping Chang-Chien 4 5,  Sufan Lin 4 5,  Hung-Wei Yang 6,  You-Lin Tain 7 8
Affiliations

Affiliations

  • 1 Department of Pharmacy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
  • 2 School of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
  • 3 Department of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung 811, Taiwan.
  • 4 Center for Environmental Toxin and Emerging-Contaminant Research, Cheng Shiu University, Kaohsiung 833, Taiwan.
  • 5 Super Micro Mass Research and Technology Center, Cheng Shiu University, Kaohsiung 833, Taiwan.
  • 6 Institute of Medical Science and Technology, National Sun Yat-sen University, Kaohsiung 804, Taiwan.
  • 7 Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
  • 8 Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
PMID: 35052651 DOI: 10.3390/antiox11010147
Abstract

Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2S-based therapy, can exert a protective effect against hypertension in an adenine-induced CKD rat model. Eight-week-old male Sprague-Dawley rats were fed with 0.5% adenine chow for 3 weeks to induce CKD. After 1 week, the rats were divided into two groups: one without and one with STS (2 g/kg body weight/day) in drinking water for 2 weeks. Treatment with STS lowered systolic and diastolic blood pressure by 7 and 9 mm Hg, respectively. Renal H2S-generating Enzyme expression was inhibited by CKD, while STS therapy increased plasma levels of H2S and thiosulfate. Additionally, restoration of nitric oxide bioavailability and rebalance of the renin-angiotensin system may contribute to the protective effects of STS. Our data suggest that the oral administration of STS improves hypertension in an adenine-induced CKD model, which brings us closer to the clinical translation of H2S-targeting therapy in CKD-induced hypertension.

Keywords

chronic kidney disease; hydrogen sulfide; hypertension; nitric oxide; renin–angiotensin system; sodium thiosulfate; symmetric dimethylarginine.

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