Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms.
Physiol Res
; 58(4): 521-527, 2009.
Article
in En
| MEDLINE
| ID: mdl-18657003
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.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Aorta, Thoracic
/
Sulfur Dioxide
/
Endothelium, Vascular
/
Muscle Relaxation
Limits:
Animals
Language:
En
Journal:
Physiol Res
Journal subject:
FISIOLOGIA
Year:
2009
Document type:
Article
Affiliation country:
China