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Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension.
Toxicol Lett 2017; 270:62-71TL

Abstract

Hydrogen sulfide (H2S) is an important gaseous signaling molecule in neuro-modulation, anti-inflammatory, anti-oxidant and anti-hypertensive effects. The paraventricular nucleus (PVN) is a major integrative nucleus in regulating BP and SNA. The aim of this study is to explore whether endogenous or exogenous H2S changed by hydroxylamine hydrochloride (HA) or GYY4137 infused in the PVN affects RSNA and MAP by regulating oxidative stress or the balance between pro-inflammatory cytokines (PICs) and anti-inflammatory cytokines in high salt-induced hypertensive rats. Male Dahl rats were fed by high-salt or normal-salt diet. At the end of the 4th week, GYY4137, HA or vehicle was microinjected into bilateral PVN for 6 weeks. The levels of MAP, HR, plasma norepinephrine (NE), reactive oxygen species (ROS), NOX2, NOX4 and IL-1β were increased significantly in high salt-induced hypertensive rats. Higher levels of these parameters were detected in the group treated by HA, but lower levels in the GYY4137 group. The trends of H2S, CBS, IL-10 and Cu/Zn SOD were opposite to the parameters described above. These findings suggest that endogenous or exogenous H2S in the PVN attenuates sympathetic activity and hypertensive response, which are partly due to decrease of ROS and PICs within the PVN in high salt-induced hypertension.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China. Electronic address: xiaojingyu621@163.com.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.Department of Endocrinology and Metabolism, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing 210029, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China. Electronic address: ykang@mail.xjtu.edu.cnor.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28185984

Citation

Liang, Yan-Feng, et al. "Hydrogen Sulfide in Paraventricular Nucleus Attenuates Blood Pressure By Regulating Oxidative Stress and Inflammatory Cytokines in High Salt-induced Hypertension." Toxicology Letters, vol. 270, 2017, pp. 62-71.
Liang YF, Zhang DD, Yu XJ, et al. Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension. Toxicol Lett. 2017;270:62-71.
Liang, Y. F., Zhang, D. D., Yu, X. J., Gao, H. L., Liu, K. L., Qi, J., ... Kang, Y. M. (2017). Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension. Toxicology Letters, 270, pp. 62-71. doi:10.1016/j.toxlet.2017.02.004.
Liang YF, et al. Hydrogen Sulfide in Paraventricular Nucleus Attenuates Blood Pressure By Regulating Oxidative Stress and Inflammatory Cytokines in High Salt-induced Hypertension. Toxicol Lett. 2017 Mar 15;270:62-71. PubMed PMID: 28185984.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension. AU - Liang,Yan-Feng, AU - Zhang,Dong-Dong, AU - Yu,Xiao-Jing, AU - Gao,Hong-Li, AU - Liu,Kai-Li, AU - Qi,Jie, AU - Li,Hong-Bao, AU - Yi,Qiu-Yue, AU - Chen,Wen-Sheng, AU - Cui,Wei, AU - Zhu,Guo-Qing, AU - Kang,Yu-Ming, Y1 - 2017/02/06/ PY - 2016/11/01/received PY - 2017/01/22/revised PY - 2017/02/05/accepted PY - 2017/2/12/pubmed PY - 2017/3/21/medline PY - 2017/2/11/entrez KW - Cystathionine beta-synthase KW - High salt-induced hypertension KW - Hydrogen sulfide KW - Inflammatory cytokines KW - Oxidative stress KW - Paraventricular nucleus SP - 62 EP - 71 JF - Toxicology letters JO - Toxicol. Lett. VL - 270 N2 - Hydrogen sulfide (H2S) is an important gaseous signaling molecule in neuro-modulation, anti-inflammatory, anti-oxidant and anti-hypertensive effects. The paraventricular nucleus (PVN) is a major integrative nucleus in regulating BP and SNA. The aim of this study is to explore whether endogenous or exogenous H2S changed by hydroxylamine hydrochloride (HA) or GYY4137 infused in the PVN affects RSNA and MAP by regulating oxidative stress or the balance between pro-inflammatory cytokines (PICs) and anti-inflammatory cytokines in high salt-induced hypertensive rats. Male Dahl rats were fed by high-salt or normal-salt diet. At the end of the 4th week, GYY4137, HA or vehicle was microinjected into bilateral PVN for 6 weeks. The levels of MAP, HR, plasma norepinephrine (NE), reactive oxygen species (ROS), NOX2, NOX4 and IL-1β were increased significantly in high salt-induced hypertensive rats. Higher levels of these parameters were detected in the group treated by HA, but lower levels in the GYY4137 group. The trends of H2S, CBS, IL-10 and Cu/Zn SOD were opposite to the parameters described above. These findings suggest that endogenous or exogenous H2S in the PVN attenuates sympathetic activity and hypertensive response, which are partly due to decrease of ROS and PICs within the PVN in high salt-induced hypertension. SN - 1879-3169 UR - https://www.unboundmedicine.com/medline/citation/28185984/Hydrogen_sulfide_in_paraventricular_nucleus_attenuates_blood_pressure_by_regulating_oxidative_stress_and_inflammatory_cytokines_in_high_salt_induced_hypertension_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-4274(17)30051-6 DB - PRIME DP - Unbound Medicine ER -