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.
Highlights
Introduction iationsHydrogen sulfide (H2 S) is a gasotransmitter, which plays an important role in several biological functions, including the renal regulation of blood pressure (BP) [1,2]
The objective of this study reported here was to examine whether sodium thiosulfate (STS) treatment can protect against chronic kidney disease (CKD)-induced hypertension and elucidate the underlying mechanism using an adenine-induced CKD
Each rat was randomly assigned to one of four treatments (n = 8 per group): normal diet (ND), diet supplemented with 0.5% adenine from 8 weeks of age for 3 weeks (CKD), normal diet with STS (2 g/kg body weight/day) in drinking water from 9 weeks of age for 2 weeks (ND + STS), and diet supplemented with 0.5% adenine from weeks 8 to 11 and STS from weeks 9 to 11 (CKD + STS)
Summary
Hydrogen sulfide (H2 S) is a gasotransmitter, which plays an important role in several biological functions, including the renal regulation of blood pressure (BP) [1,2]. Hypertension and chronic kidney disease (CKD) both are common diseases all over the world [3], being closely connected to each other. Emerging evidence suggests that a reduction in H2 S synthesis may be a key mechanism underlying hypertension and kidney disease [1,2,4]. A mismatch of vasodilators, such as H2 S and nitric oxide (NO), and vasoconstrictors, such as angiotensin II (Ang II), in favor of the latter, may lead to hypertension [5,6]. H2 S-based modalities have been developed for therapeutic protection against hypertension and kidney disease [6,7].
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