To investigate the effects of hydrogen sulfide (H2S) on vascular inflammation and blood pressure in spontaneously hypertensive rats (SHR).
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.
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).
H2S might attenuate the development of hypertension through by attenuating vascular inflammation reactions.