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内源性变力因子诱导的血管平滑肌内皮依赖性舒张。

Endogenous inotropic factor-induced endothelium-dependent relaxation of vascular smooth muscle.

作者信息

Han C, Khatter J C

机构信息

Department of Internal Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

Br J Pharmacol. 1996 May;118(2):228-32. doi: 10.1111/j.1476-5381.1996.tb15391.x.

DOI:10.1111/j.1476-5381.1996.tb15391.x
PMID:8735619
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1909640/
Abstract
  1. Possible contractile or relaxation effects of an endogenous inotropic factor (EIF) isolated and purified from porcine heart left ventricle were examined in rat isolated aortic ring preparations. 2. EIF induced a dose-dependent relaxation of the rat isolated aortic ring preparation pre-contracted with 0.4 microM phenylephrine (PE); 200 microliters (in 5 ml bath) of EIF caused relaxation of aortic rings by as much as 67.4 +/- 4.5%. In another set of experiments, in the presence of 100 microliters EIF, the PE concentration-response contractile curve shifted to the right, the maximal contractile force was reduced by as much as 32.8% and the EC50 of PE increased from 0.2 to 0.3 microM. 3. The relaxation effect of EIF was demonstrated to be endothelium-dependent. Additional experiments demonstrated that EIF-induced relaxation in an isolated aortic ring could be inhibited by 2 microM NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, suggesting the involvement of nitric oxide in EIF-induced relaxation of the muscle. 4. Atropine (0.2 microM) or indomethacin (10 microM) had no significant effect on EIF-induced relaxation. 5. These data suggest that EIF, a novel endogenous inotrope from porcine myocardium, also acts as an endothelium-dependent vasodilator substance mediating relaxation in the rat isolated aorta mainly by release of nitric oxide. The possibility of EIF acting through muscarinic receptor and the involvement of prostacyclin were excluded.
摘要
  1. 从猪心脏左心室分离并纯化出一种内源性变力因子(EIF),研究了其对大鼠离体主动脉环标本可能产生的收缩或舒张作用。2. EIF可使预先用0.4微摩尔苯肾上腺素(PE)预收缩的大鼠离体主动脉环标本产生剂量依赖性舒张;200微升(5毫升浴槽中)EIF可使主动脉环舒张多达67.4±4.5%。在另一组实验中,在存在100微升EIF的情况下,PE浓度-反应收缩曲线右移,最大收缩力降低多达32.8%,PE的半数有效浓度(EC50)从0.2微摩尔增加到0.3微摩尔。3. EIF的舒张作用被证明是内皮依赖性的。进一步实验表明,一氧化氮合酶抑制剂2微摩尔N-硝基-L-精氨酸甲酯可抑制EIF诱导的离体主动脉环舒张,提示一氧化氮参与了EIF诱导的肌肉舒张。4. 阿托品(0.2微摩尔)或吲哚美辛(10微摩尔)对EIF诱导的舒张无显著影响。5. 这些数据表明,EIF是一种来自猪心肌的新型内源性变力因子,它还作为一种内皮依赖性血管舒张物质,主要通过释放一氧化氮介导大鼠离体主动脉的舒张。排除了EIF通过毒蕈碱受体发挥作用的可能性以及前列环素的参与。

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引用本文的文献

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An endogenous positive inotropic factor (EPIF) from porcine heart: its effects on sarcoplasmic reticular (SR) Ca2+ metabolism.来自猪心脏的内源性正性肌力因子(EPIF):其对肌浆网(SR)钙代谢的影响。
Mol Cell Biochem. 1997 Nov;176(1-2):163-8.

本文引用的文献

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Pharmacological characterization of the activity of endogenous inotropic factor from porcine left ventricle.猪左心室内源性正性肌力因子活性的药理学特性
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