title: Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms.
abstract: This study aimed to investigate the vasoactivity of sulfur dioxide (SO2), a novel gas identified from vascular tissue, in rat thoracic aorta. The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers. After equilibrium, the rings were gradually stretched to a resting tension. Isometric tension was recorded under the treatments with vasoconstrictors, SO2 derivatives, and various drugs as pharmacological interventions. In endothelium-intact aortic rings constricted by 1 microM phenylephrine (PE), SO2 derivatives (0.5-8 mM) caused a dose-dependent relaxation. Endothelium removal and a NOS inhibitor L-NAME reduced the relaxation to low doses of SO2 derivatives, but not that to relatively high doses (>or=2 mM). In endothelium-denuded rings, SO2 derivatives attenuated vasoconstriction induced by high K+ (60 mM) or CaCl2 (0.01-10 mM). The relaxation to SO2 derivatives in PE-constricted rings without endothelium was significantly inhibited by blockers of ATP-sensitive K+(KATP) and Ca2+-activated K+ (KCa) channels, but not by those of voltage-dependent K+ channels, Na+- K+-ATPase or Na+-Ca2+ exchanger. SO2 relaxed vessel tone via endothelium-dependent mechanisms associated with NOS activation, and via endothelium-independent mechanisms dependent on the inhibition of voltage-gated Ca2+ channels, and the opening of KATP and KCa channels.
authors.affiliation: Department of Physiology, Second Military Medical University, Shanghai, China.
authors.forename: Y-K
authors.initials: YK
authors.lastname: Wang
authors.forename: A-J
authors.initials: AJ
authors.lastname: Ren
authors.forename: X-Q
authors.initials: XQ
authors.lastname: Yang
authors.forename: L-G
authors.initials: LG
authors.lastname: Wang
authors.forename: W-F
authors.initials: WF
authors.lastname: Rong
authors.forename: C-S
authors.initials: CS
authors.lastname: Tang
authors.forename: W-J
authors.initials: WJ
authors.lastname: Yuan
authors.forename: L
authors.initials: L
authors.lastname: Lin
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000502:physiology; D015220:Calcium Channels / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013458:Sulfur Dioxide / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014665:Vasodilator Agents; D013458:Sulfur Dioxide