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2015 ; 2015
(ä): 927686
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Superoxide Mediates Depressive Effects Induced by Hydrogen Sulfide in Rostral
Ventrolateral Medulla of Spontaneously Hypertensive Rats
#MMPMID26078823
Yu H
; Xu H
; Liu X
; Zhang N
; He A
; Yu J
; Lu N
Oxid Med Cell Longev
2015[]; 2015
(ä): 927686
PMID26078823
show ga
Hydrogen sulfide (H2S) plays a crucial role in the regulation of blood pressure
and oxidative stress. In the present study, we tested the hypothesis that H2S
exerts its cardiovascular effects by reducing oxidative stress via inhibition of
NADPH oxidase activity in the rostral ventrolateral medulla (RVLM). We examined
cell distributions of cystathionine-?-synthase (CBS) and effects of H2S on
reactive oxygen species (ROS) and mean arterial blood pressure (MAP) in
spontaneously hypertensive rats (SHRs). We found that CBS was expressed in
neurons of the RVLM, and the expression was lower in SHRs than in Wistar-Kyoto
rats. Microinjection of NaHS (H2S donor), S-adenosyl-l-methionine (SAM, a CBS
agonist), or Apocynin (NADPH oxidase inhibitor) into the RVLM reduced the ROS
level, NADPH oxidase activity, and MAP, whereas microinjection of hydroxylamine
hydrochloride (HA, a CBS inhibitor) increased MAP. Furthermore,
intracerebroventricular infusion of NaHS inhibited phosphorylation of p47(phox),
a key step of NADPH oxidase activation. Since decreasing ROS level in the RVLM
reduces MAP and heart rate and increasing H2S reduces ROS production, we conclude
that H2S exerts an antihypertensive effect via suppressing ROS production. H2S,
as an antioxidant, may be a potential target for cardiovascular diseases.