An investigation of the mechanisms of hydrogen sulfide-induced vasorelaxation in rat middle cerebral arteries

摘要: Hydrogen sulfide (H2S) is an endogenous mediator with peripheral vasorelaxant effects; however, the mechanism of H2S-induced vasorelaxation in cerebral blood vessels has not been extensively studied. Vasorelaxation studies were performed on middle arteries from male Sprague Dawley rats using wire myography. Immunofluorescence staining was used to detect presence H2S-producing enzyme cystathionine-γ-lyase (CSE). CSE present endothelium and smooth muscle arteries. The substrate, l-cysteine, induced that sensitive inhibitor dl-propargylglycine. This relaxation independent endothelium, suggesting H2S produced vascular muscle. donor, sodium hydrogen (NaHS; 0.1–3.0 mM) concentration-dependent relaxation, which unaffected by removal. Nifedipine (3 μM) significantly reduced maximum elicited NaHS. Inhibiting potassium (K+) conductance 50 mM K+ attenuated NaHS-induced selective blockers ATP (KATP), calcium (KCa), voltage dependent (KV), or inward rectifier (Kir) channels alone combination did affect response 4,4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS; 300 μM) caused a significant rightward shift NaHS concentration-response curve, but this effect could be explained inhibition Cl− Cl−/ HCO 3 − exchange, as blockade these mechanisms had no effect. These findings suggest can regulate function. H2S-mediated DIDS partly mediated l-type channels, additional contribution K KATP, KCa, KV, Kir subtypes.