Hydrogen Sulfide Inhibits High-Salt Diet-Induced Myocardial Oxidative Stress and Myocardial Hypertrophy in Dahl Rats

Abstract

The study aimed to examine the protective effect of hydrogen sulfide (H2S) on high-salt-induced oxidative stress and myocardial hypertrophy in salt-sensitive (Dahl) rats. Thirty male Dahl rats and 40 SD rats were included in the study. They were randomly divided into Dahl control (Dahl + NS), Dahl high salt (Dahl + HS), Dahl + HS + NaHS, SD + NS, SD + HS, SD + HS + NaHS, and SD + HS + hydroxylamine (HA). Rats in Dahl + NS and SD + NS groups were given chow with 0.5% NaCl and 0.9% normal saline intraperitoneally daily. Myocardial structure, α-myosin heavy chain (α-MHC) and β-myosin heavy chain (β-MHC) expressions were determined. Endogenous myocardial H2S pathway and oxidative stress in myocardial tissues were tested. Myocardial H2S pathway was downregulated with myocardial hypertrophy featured by increased heart weight/body weight and cardiomyocytes cross-sectional area, decreased α-MHC and increased β-MHC expressions in Dahl rats with high-salt diet (all P < 0.01), and oxidative stress in myocardial tissues was significantly activated, demonstrated by the increased contents of hydroxyl radical, malondialdehyde and oxidized glutathione and decreased total antioxidant capacity, carbon monoxide, catalase, glutathione, glutathione peroxidase, superoxide dismutase (SOD) activities and decreased SOD1 and SOD2 protein expressions (P < 0.05, P < 0.01). However, H2S reduced myocardial hypertrophy with decreased heart weight/body weight and cardiomyocytes cross-sectional area, increased α-MHC, decreased β-MHC expressions and inhibited oxidative stress in myocardial tissues of Dahl rats with high-salt diet. However, no significant difference was found in H2S pathway, myocardial structure, α-MHC and β-MHC protein and oxidative status in myocardial tissues among SD + NS, SD + HS, and SD + HS + NaHS groups. HA, an inhibitor of cystathionine β-synthase, inhibited myocardial H2S pathway (P < 0.01), and stimulated myocardial hypertrophy and oxidative stress in SD rats with high-salt diet. Hence, H2S inhibited myocardial hypertrophy in high salt-stimulated Dahl rats in association with the enhancement of antioxidant capacity, thereby inhibiting oxidative stress in myocardial tissues.

Cooperative Oxygen Sensing by the Kidney and Carotid Body in Blood Pressure Control

“…Hydrogen sulfide, H 2 S, a gaseous endogenous signaling molecule, is increasingly identified to be involved in numerous cardiovascular (patho)physiology (Snijder et al, 2014 , 2015 ; Xie et al, 2016 ; Huang et al, 2017 ; Merz et al, 2017 ). In the kidney, H 2 S exerts significant diuretic, natriuretic and kaliuretic effects by raising glomerular filtration rate and inhibiting tubular sodium re-absorption (Xia et al, 2009 ).…”

The Role of Hydrogen Sulfide on Cardiovascular Homeostasis: An Overview with Update on Immunomodulation

“…So far, a plethora of investigations have been performed on therapeutic values of H 2 S in cardiovascular diseases, which reveal that H 2 S at physiological levels has an important role in cardiovascular homeostasis, and inhibitors of endogenous H 2 S production or H 2 S donors exert significant effects in cardiovascular diseases, including heart failure, ischemic myocardium, atherosclerosis, and hypertension ( Yang et al, 2008 ; Wang et al, 2009 ; Calvert et al, 2010 ; Miao et al, 2016a ). Furthermore, empirical studies have elucidated several mechanisms of H 2 S-mediated cardiovascular protective activities, which include, but are not restricted to, anti-oxidation ( Chang et al, 2008 ; Wang et al, 2009 ; Huang et al, 2017 ), anti-apoptosis ( Yan et al, 2017 ), ion channel regulation ( Pan et al, 2008 ; Ma et al, 2015 ), pro-angiogenesis ( Cai et al, 2007 ), and anti-inflammation ( Pan et al, 2011 ; Wallace and Wang, 2015 ). The realization of biological importance of H 2 S in numerous cells, tissues and organs is now shedding light on the pathogenesis of various cardiovascular diseases, and paving the way for innovative therapeutic interventions ( Wallace and Wang, 2015 ; Zheng et al, 2017 ).…”

Protective Mechanism of Hydrogen Sulfide against Chemotherapy-Induced Cardiotoxicity

“…Once produced, H 2 S is broken down rapidly and participates in many pathophysiological processes (Tang et al, 2006 ; Du et al, 2011 , 2014 ; Sun et al, 2011 ; Altaany et al, 2014 ; Yang and Wang, 2015 ; Bian et al, 2016 ; Cao and Bian, 2016 ; Panthi et al, 2016 ). More importantly, recent evidence shows that H 2 S may play cytoprotective role in heart diseases (Shen et al, 2015 ; Liu et al, 2016a ; Szabo, 2016 ; Huang et al, 2017 ). Here, we mainly reviewed the cardioprotective role of H 2 S in chemotherapy and its possible mechanisms.…”