TY - JOUR
T1 - Sodium Thiosulfate Improves Hypertension in Rats with Adenine-Induced Chronic Kidney Disease
AU - Hsu, Chien Ning
AU - Hou, Chih Yao
AU - Chang-Chien, Guo Ping
AU - Lin, Sufan
AU - Yang, Hung Wei
AU - Tain, You Lin
N1 - Funding Information:
This work was supported by grant CORPG8L0121 from the Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan, and National Sun Yat-sen University, Kaohsiung, Taiwan. We would like to thank the Center for Environmental Toxin and Emerging Contaminant Research and the Super Micro Mass Research and Technology Center, Cheng Shiu University, Kaohsiung for technical support.
Funding Information:
Funding: This work was supported by grant CORPG8L0121 from the Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan, and National Sun Yat-sen University, Kaohsiung, Taiwan.
Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2022/1
Y1 - 2022/1
N2 - Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2 S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2 S-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 H2 S-generating enzyme expression was inhibited by CKD, while STS therapy increased plasma levels of H2 S 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 H2 S-targeting therapy in CKD-induced hypertension.
AB - Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2 S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2 S-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 H2 S-generating enzyme expression was inhibited by CKD, while STS therapy increased plasma levels of H2 S 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 H2 S-targeting therapy in CKD-induced hypertension.
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U2 - 10.3390/antiox11010147
DO - 10.3390/antiox11010147
M3 - Article
AN - SCOPUS:85122700377
SN - 2076-3921
VL - 11
JO - Antioxidants
JF - Antioxidants
IS - 1
M1 - 147
ER -