Abstract

H2S signaling pathways interact with NO signaling pathways. To contribute to the understanding of the cross-talk between these pathways, we studied H2S induced NO release from nitroso-compounds in vitro and the biological effects of the reaction products. It was observed that H2S released NO from brain homogenate or cultured cells, indicating that biological systems contain nitroso-compounds from which H2S can induce NO release. In an in vitro model, the H2S donor Na2S decomposes S-nitrosoglutation (GSNO), which results in the formation of polysulfides S n 2 - and (SSNO−). Bolus application of a S n 2 - and H2S mixture at microM concentrations had significantly pronounced effect in vivo on rat hemodynamic parameters compared to H2S alone. In ex-vivo models, SSNO− relaxed phenylephrine induced aortic and mesenteric ring contraction. Its effect was faster and more pronounced in comparison to GSNO. As detected by spin trap EPR technique, SSNO− released NO faster than GSNO and scavenged the cPTIO radical. S n 2 - and SSNO− both modulated the activities of calcium RyR2 and chloride channels. In conclusion, the exogenously produced products of H2S-GSNO interaction, S n 2 - and SSNO−, had biological effects in vivo, ex-vivo and in vitro. However, detection of possible endogenous products of H2S-GSNO interactions is a challenge for future research. This work was supported by APVV-0074-11 and VEGA 2/0050/13.

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