Sulfur Dioxide Relaxes Rat Aorta by Endothelium-Dependent and -Independent Mechanisms
Sulfur Dioxide Relaxes Rat Aorta by Endothelium-Dependent and -Independent Mechanisms
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二氧化硫通过内皮依赖性和独立机制放松大鼠主动脉
DOI：
10.33549/physiolres.931456
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发表时间：
2009-01-01
影响因子：
2.1
通讯作者：
Lin, L.
中科院分区：
文献类型：
--
作者：
Wang, Y. -K.;Ren, A. -J.;Lin, L.
本文旨在研究大鼠胸主动脉血管组织中二氧化硫（SO2）的血管活性。分离胸主动脉，切成环，装入器官浴室。平衡后，环逐渐拉伸到静息张力。用血管收缩剂、二氧化硫衍生物和各种药物作为药物干预，记录等长张力。在1 μ M苯肾上腺素（PE）收缩的内皮完整的主动脉环中，SO2衍生物（0.5 - 8 mM）引起剂量依赖性松弛。内皮去除和NOS抑制剂L-NAME降低了SO2衍生物在低剂量时的弛豫，而在相对高剂量（>= 2 mM）时则没有。在内皮剥蚀环中，SO2衍生物可减弱高K+ (60 mM)或CaCl2 （0.01-10 mM）引起的血管收缩。atp敏感的K+ (K- atp)和Ca2+激活的K+ (K- ca)通道阻滞剂显著抑制无内皮pe收缩环对SO2衍生物的弛缓，而电压依赖性K+通道、Na+-K+- atp酶或Na+-Ca2+交换剂的阻滞剂则不起作用。SO2通过与NOS激活相关的内皮依赖性机制，以及依赖于抑制电压门控Ca2+通道、K-ATP和K-Ca通道开放的内皮非依赖性机制来放松血管张力。
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 mu M 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 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+ (K-ATP) and Ca2+-activated K+ (K-Ca) 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 K-ATP and K-Ca channels.