Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms

Title:

Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms

Creator:

Y.-K. Wang, Ren, A.-J., Yang, X.-O., Wang, L.-G., Rong, W.-F., Tang, C.-S., Yuan, W.-J., and Lin, L.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:356ce8bd-b1d7-43c2-a086-920b1e4aed68
uuid:356ce8bd-b1d7-43c2-a086-920b1e4aed68

Subject:

Fyziologie člověka a srovnávací fyziologie, oxid siřičitý, iontové kanály, endotel, aorta, krysa obecná, sulphur dioxide, ion channels, endothelium, Rattus rattus, vasorelaxation, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

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 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 (≥ 2 mM). In endothelium-denuded rings, SO2 derivatives attenuat ed 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., Y.-K- Wang., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2009 Volume:58 | Number:4

Harvested from:

CDK

Metadata only:

false