[Hypotensive effects of hydrogen sulfide via attenuating vascular inflammation in spontaneously hypertensive rats].
OBJECTIVE
To investigate the effects of hydrogen sulfide (H2S) on vascular inflammation and blood pressure in spontaneously hypertensive rats (SHR).


METHODS
Four weeks old male SHR rats were treated with saline (control, n = 7), sodium hydrosulfide (NaHS, a H2S donor, n = 7) and propargylglycine (PPG, endogenous H2S production inhibitor, n = 6) for 5 weeks. Age-natched male Wistar Kyoto (WKY) rats served as normotensive controls (n = 8). Five weeks later, systolic blood pressure (SBP) was measured in conscious and quiet rats by means of the standard tail-cuff method. The protein expressions of intercellular adhesive molecule-1 (ICAM-1), nuclear transcriptional factor-kappaB p65 (NF-kappaB p65) and inhibitor of nuclear transcriptional factor-kappaB (IkappaB-alpha) in thoracic aorta of rats were detected by immunohistochemical assay, while the expression of ICAM-1 mRNA in thoracic aorta of rats were investigated by in situ hybridization.


RESULTS
SBP of control SHR rats was significantly higher than that of WKY rats (P < 0.05) accompanied by significantly upregulated expressions of ICAM-1 mRNA, ICAM-1 protein, NF-kappaB p65 protein in aortic endothelial cells (all P < 0.01), while the expression of IkappaB-alpha protein in aortic endothelial cells in SHR control group was significantly lower than that of WKY control group (P < 0.01). NaHS treated SHR rats showed significantly reduced SBP and downregulated expressions of ICAM-1 mRNA, ICAM-1, NF-kappaB p65 in aortic endothelial cells and upregulated expression of IkappaB-alpha protein in aortic endothelial cells compared to untreated control SHR rats (all P < 0.05). In SHR rats treated with PPG, the expressions of ICAM-1 mRNA, ICAM-1 protein, NF-kappaB p65 protein in aortic endothelial cells were further increased while the expression of IkappaB-alpha protein further decreased compared with control SHR rats (all P < 0.05).


CONCLUSIONS
H2S might attenuate the development of hypertension through by attenuating vascular inflammation reactions.
Jin
Hong-fang
HF
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Sun
Yan
Y
Liang
Jia-min
JM
Tang
Chao-shu
CS
DU
Jun-bao
JB
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism*; D051550:I-kappa B Kinase / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D051996:Transcription Factor RelA / Q000378:metabolism
D012333:RNA, Messenger; D051996:Transcription Factor RelA; D018799:Intercellular Adhesion Molecule-1; D051550:I-kappa B Kinase; D006862:Hydrogen Sulfide