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H 2 S Prevents Cyclosporine A-Induced Vasomotor Alteration in Rats.

Authors :: Ping NN
Mi YN
Liu DZ
Zhang S
Chen JG
Cao YX
Source :: Cardiovascular toxicology [Cardiovasc Toxicol] 2017 Jul; Vol. 17 (3), pp. 287-296.
Publication Year :: 2017
Abstract: Cyclosporine A (CsA) induces hypertension after transplantation. Hydrogen sulfide (H <subscript>2</subscript> S) was found to have hypotensive/vasoprotective effects in the cardiovascular system. The present study aims to investigate the role of H <subscript>2</subscript> S on CsA-induced vascular function disorder in rats. Rats were subcutaneously injected with CsA 25 mg/kg for 21 days. Blood pressure was measured by the tail-cuff method. Vasomotion was determined using a sensitive myograph. Western blotting and immunohistochemistry were used to quantify the protein expression of endothelin type A (ET <subscript>A</subscript> ) receptor and essential MAPK pathway molecules. Vascular superoxide anion production and serum contents of malondialdehyde were determined. The results showed that sodium hydrosulfide (NaHS), a H <subscript>2</subscript> S donor, significantly attenuated the increase of blood pressure and contractile responses, and the upregulation of ET <subscript>A</subscript> receptor induced by CsA. In addition, NaHS could restore the CsA decreased acetylcholine-induced vasodilatation. Furthermore, NaHS blocked the CsA-induced elevation of reactive oxygen species level, extracellular signal-regulated kinase and p38 MAPK activities. In conclusion, H <subscript>2</subscript> S prevents CsA-induced vasomotor dysfunction. H <subscript>2</subscript> S attenuates CsA-induced ET <subscript>A</subscript> receptor upregulation, which may be associated with MAPK signal pathways. H <subscript>2</subscript> S ameliorates endothelial-dependent relaxation, which may be through antioxidant activity.