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硫化氫收縮大鼠腦動脈
來源: | 作者: | 發布時間:2014-4-15 16:21:13

硫化氫收縮大鼠腦動脈
李森,平娜娜,肖雪,曹永孝
基金項目:高等學校博士學科點專項科研基金(20100201110054) 作者簡介:李森(1984-),男,在讀博士生,主要研究方向:血管藥理學 通信聯系人:曹永孝(1957-),男,博士生導師,主要研究方向:血管藥理學;中藥組分與作用靶點;環境疾病與受體研究.

(西安交通大學醫學院,西安 710061)

摘要:目的 新的氣體信號分子硫化氫對腦血管的作用尚不明確,本文研究硫化氫收縮大鼠腦血管的作用及其機制。方法 用NaHS作為硫化氫供體,用微血管張力描記儀記錄血管張力,用硫電極法測定硫化氫含量。結果 NaHS可濃度依賴性地收縮大鼠腦基底動脈;β2受體激動劑沙丁胺醇、腺苷酸環化酶抑制劑毛喉素均可增強NaHS對腦基底動脈的收縮作用,NaHS孵育可減弱沙丁胺醇或毛喉素對5-HT預收縮腦基底動脈的舒張作用;α2受體阻斷劑蘿芙素、cAMP類似物8B-cAMP均可減弱NaHS對腦基底動脈的收縮作用;一氧化氮合酶抑制劑L-NAME可增強NaHS對腦基底動脈的收縮作用,在L-NAME存在下,NaHS則可以減弱毛喉素對大鼠腦基底動脈的舒張作用;去除血管內皮可增強NaHS的腦血管收縮作用,而在毛喉素存在下,去除血管內皮會減弱NaHS的腦血管收縮作用;鉀ATP通道阻斷劑格列苯脲不影響NaHS對腦基底動脈的收縮作用。L型鈣通道阻斷劑硝苯地平可減弱NaHS對腦基底動脈的收縮作用。L型鈣通道開放劑Bay K 8644不影響NaHS對腦基底動脈的收縮作用;與Krebs液相比,NaHS在不含碳酸氫根離子的HEPES液中的腦血管收縮作用減弱,而陰離子交換抑制劑DIDS和氧自由基抑制劑Tiron也可減弱NaHS對腦基底動脈的收縮作用。自發性高血壓大鼠血漿和腦組織勻漿液中的硫化氫含量低于SD大鼠。結論 硫化氫可收縮大鼠腦基底動脈,這一作用可能與H2S降低腦血管平滑肌cAMP,調節碳酸氫根20 與氧自由基在細胞膜上的轉運及隨后氧自由基與NO的反應等機制有關。
關鍵詞:藥理學;硫化氫;腦動脈;環磷酸腺苷;血管收縮
中圖分類號:R965
Hydrogen sulfide contracts rat cerebral artery in vitro
LI Sen, PING Nana, XIAO Xue, CAO Yongxiao
(College of Medicine,Xi'an Jiaotong University,Xi'an 710061)
Abstract: OBJECTIVE This study was designed to examine that vasoconstrictive effect of hydrogen sulfide, a new endogenous mediator on rat cerebral artery. METHODS NaHS was used as the donor of H2S. The vasoconstrictive effect of NaHS on rat cerebral artery was measured by wire myograph. H2S production was measured by sulfur electrode. RESULTS NaHS induced a concentration-dependently vasoconstriction on rat cerebral artery. Salbutamol, a β-adrenoceptor agonists, and forskolin, a selective adenylyl cyclase activator produced stronger vasoconstriction caused by NaHS on rat cerebral artery, respectively. Pretreatment with NaHS also significantly attenuated the vasorelaxant effect of salbutamol and forskolin on 5-HT precontracted rat cerebral  artery. Rauwolscine, a α2-adrenoceptor agonists, and 8B-cAMP, a cell permeable analog of cAMP produced weaker vasoconstriction caused by NaHS on rat cerebral artery, respectively. However, NaHS produced stronger vasoconstriction in the presence of L-NAME, a nitric oxide synthase inhibitor, or in the endothelium-denuded rat cerebral artery. NaHS also produced weaker vasodilation caused by forskolin in the presence of L-NAME but not in endothelium-denuded rat cerebral artery. Blockade of ATP-sensitive potassium channels with glibenclamide failed to attenuate the vasoconstriction induced by NaHS. Nifedpine, a specific L-type Ca2+ channel inhibitor, reduced the vasoconstriction caused by NaHS while Bay K 8644, a specific L-type Ca2+ channel agonist, failed to attenuate the vasoconstriction caused by NaHS on rat cerebral artery . In HEPES and Krebs buffers, the HCO3- dependent effect was specific to H2S. Blockade of anion  exchanger-2 activity with DIDS or with HCO3- free solution abolished the vasoconstrictive effect of NaHS. Tiron,a ROS scavenger, produced weaker vasoconstriction caused by NaHS on rat cerebral artery.The plasma H2S concentration and H2S production in brain tissues both decreased in SHR compared to SD rats. CONCLUSION H2S contracts rat cerebral artery. The vasoconstrictive effect of H2S may be involved in the adenyly cyclase/cAMP pathway. H2S also stimulates anion exchanger to transport extracellular HCO3- in exchange for intracellular superoxide anions which may further inactivate NO to induce vasoconstriction.
Key words: pharmacology; hydrogen sulfide ; cerebral artery ; cAMP; vasoconstrictive effect

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