Role of hydrogen sulfide in sulfur dioxide production and vascular regulation

Both hydrogen sulfide (H(2)S) and sulfur dioxide (SO(2)) are produced endogenously from the mammalian metabolic pathway of sulfur-containing amino acids and play important roles in several vascular diseases. However, their interaction during the control of vascular function has not been fully clear. Here, we investigated the potential role of H(2)S in SO(2) production and vascular regulation in vivo and in vitro. Wistar rats were divided into the vehicle, SO(2), DL-propargylglycine (PPG) + SO(2), β-cyano-L-alanine (BCA) + SO(2) and sodium hydrosulfide (NaHS) + SO(2) groups. SO(2) donor was administered with or without pre-administration of PPG, BCA or NaHS for 30 min after blood pressure was stabilized for 1 h, and then, the change in blood pressure was detected by catheterization via the common carotid artery. Rat plasma SO(2) and H(2)S concentrations were measured by high performance liquid chromatography and sensitive sulfur electrode, respectively. The isolated aortic rings were prepared for the measurement of changes in vasorelaxation stimulated by SO(2) after PPG, BCA or NaHS pre-incubation. Results showed that the intravenous injection of SO(2) donors caused transient hypotension in rats compared with vehicle group. After PPG or BCA pretreatment, the plasma H(2)S content decreased but the SO(2) content increased markedly, and the hypotensive effect of SO(2) was significantly enhanced. Conversely, NaHS pretreatment upregulated the plasma H(2)S content but reduced SO(2) content, and attenuated the hypotensive effect of SO(2). After PPG or BCA pre-incubation, the vasorelaxation response to SO(2) was enhanced significantly. While NaHS pre-administration weakened the SO(2)-induced relaxation in aortic rings. In conclusion, our in vivo and in vitro data indicate that H(2)S negatively controls the plasma content of SO(2) and the vasorelaxant effect under physiological conditions.