Abstract

Objectives: This study aims to explore effect of homocysteine (Hcy) and hydrogen sulfide (H2S) on blood pressure and possible mechanism in rats with hyperhomocysteine. Methods: Wistar and SHR rats were both divided into 4 groups. Control group was feed with regular diet and Hcy group was feed with high methionine diet for 8 weeks. For Folic acid 1 group, folic acid was added into the high methionine diet food for 8 weeks. Folic acid 2 group rats were raised with high methionine diet for the first 8 weeks then replaced the diet with folic acid food for another 4 weeks. Blood pressure of rats in each group were measured and recorded with non-invasive tail blood pressure measuring instrument. After anaesthesia, blood samples were obtained from heart of rats with a disposable sterilized syringe. Radiation immunoassay kits were applied to test level of angiotensin II in plasma. H2S in serum was examined with a sensitive sulphur electrode and homocysteine was determined by enzyme-linked immunosorbent assay. Expression of cystathionine-γ lyase (CSE) and angiotensin converting enzyme I (ACE I) was determined by western-blot. SPSS 22.0 was applied in statistical analysis. Results: Wistar rat blood pressure significantly increased with an elevation of plasma Hcy and decreased after folic acid treatment. With elevation of Hcy in SHR rats, serum AngII level declined and ACE I level in kidney increased, this change could be eliminated after folic acid treatment. Both serum H2S and kidney CSE showed negative correlation with Hcy. The two folic acid treatment plans had similar influence on reducing plasma Hcy. Conclusion: Endogenous H2S could be a mediator in the process of blood pressure responding to Hcy change. Preventive folic acid prescription could achieve the same effect with less sufferance.

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