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- Title
Sulfur Dioxide Relaxes Rat Aorta by Endothelium-Dependent and -Independent Mechanisms.
- Authors
Wang, Y.-K.; Ren, A.-J.; Yang, X.-Q.; Wang, L.-G.; Rong, W.-F.; Tang, C.-S.; Yuan, W.-J.; Lin, L.
- 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 μM phenylephrine (PE), SO2 derivatives (0.5 - 8 mM) caused a dosedependent 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 (≥ 2 mM). In endotheliumdenuded 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 ATPsensitive 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 endotheliumdependent 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.
- Subjects
SULFUR dioxide; ENDOTHELIUM; AORTA; BLOOD circulation; RATS
- Publication
Physiological Research, 2009, Vol 58, Issue 4, p521
- ISSN
0862-8408
- Publication type
Article
- DOI
10.33549/physiolres.931456