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cAMP-PKA信号转导在SO2衍生物舒张血管中作用

Vasodilatation of SO2 derivatives and cAMP-PKA signal transduction

  • 摘要: 目的 研究环腺苷酸单磷酸-蛋白激酶A(cAMP-PKA)信号转导系统在SO2衍生物舒张血管中的作用.方法 当SO2衍生物诱发该血管环舒张时,采用放射免疫法检测血管环组织环腺苷酸单磷酸(cAMP)、环鸟苷酸单磷酸(cGMP)、前列环素(PGI2)和血栓素(TXA2)的稳定代谢产物6-酮-前列腺素F1a(6-keto-PGF1a,6-keto)和血栓素B2(TXB2)的含量,并用32P掺入底物法测定组织中的蛋白激酶A(PKA)活性.结果 SO2衍生物可引起血管组织中cAMP、6-kceto(即PGI2)含量及PKA活性增加,其增加程度与内皮无关;SO2衍生物不能引起血管环cGMP和TXB2含量的变化,但可引起cAMP/cGMP和6-keto/TXB2比值显著升高.结论 SO2衍生物可使PGI2-cAMP-PKA信号通路活化,这可能是SO2导致血管舒张的机制之一.

     

    Abstract: Objective To study the role of cAMP-PKA signal transduction pathway on vasodilatation of rataorticrings caused by SO2 der ivatives.Methods Levels of cAMA,cGMP,6-keto-PGF 1A,TXB2 in the isolated aor tic rings of rats were deter mined by radioimmunoassay.PKA activity was assayed by transferr ing phosphorus(32p)into the biotinylated peptide Kemptide,the most specific substrate for PKA.Results Levels of cAMP,6-keto(PGI2)and PKA activity in isolated aorticrings were increased by SO2 derivat ives in a dose-dependent way,which wer e independent of endothelium;No change of cGMP and TXB2 in rings with or without endothelium were observed;cAMP/cGMP and 6-keto/TXB2,ratios were increased significantly.Conclusion The relaxation effect on the rings caused by SO2 der ivatives might be mediated partly by the PGI2-cAMP-PKA signal transduction pathway.SO/SO2,the precursors of SO2 derivatives,might be a newcellular gas signal molecule,more studies are needed to understand its physiological role.

     

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