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Hydrogen sulfide-induced relaxation of resistance mesenteric artery beds of rats

Department of Physiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 5E5

Submitted 6 April 2004 ; accepted in final form 4 June 2004

Hydrogen sulfide (H₂S) has been shown recently to function as an important gasotransmitter. The present study investigated the vascular effects of H₂S, both exogenously applied and endogenously generated, on resistance mesenteric arteries of rats and the underlying mechanisms. Both H₂S and NaHS evoked concentration-dependent relaxation of in vitro perfused rat mesenteric artery beds (MAB). The sensitivity of MAB to H₂S (EC₅₀, 25.2 ± 3.6 µM) was about fivefold higher than that of rat aortic tissues. Removal of endothelium or coapplication of charybdotoxin and apamin to endothelium-intact MAB significantly reduced the vasorelaxation effects of H₂S. The H₂S-induced relaxation of MAB was partially mediated by ATP-sensitive K⁺ (K_ATP) channel activity in vascular smooth muscle cells. Pinacidil (EC₅₀, 1.7 ± 0.1 µM, n = 6) mimicked, but glibenclamide (10 µM, n = 6) suppressed, the vasorelaxant effect of H₂S. K_ATP channel currents in isolated mesenteric artery smooth muscle cells were significantly augmented by H₂S. L-Cysteine, a substrate of cystathionine--lyase (CSE), at 1 mM increased endogenous H₂S production by sixfold in rat mesenteric artery tissues and decreased contractility of MAB. dl-Propargylglycine (a blocker of CSE) at 10 µM abolished L-cysteine-dependent increase in H₂S production and relaxation of MAB. Our results demonstrated a tissue-specific relaxant response of resistance arteries to H₂S. The stimulation of K_ATP channels in vascular smooth muscle cells and charybdotoxin/apamin-sensitive K⁺ channels in vascular endothelium by H₂S represents important cellular mechanisms for H₂S effect on MAB. Our study also demonstrated that endogenous CSE can generate sufficient H₂S from exogenous L-cysteine to cause vasodilation. Future studies are merited to investigate direct contribution of endogenous H₂S to regulation of vascular tone.

cystathionine--lyase; ATP-sensitive K⁺ channels; smooth muscle cells

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